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1.
Frontiers of Medicine ; (4): 25-38, 2022.
Article in English | WPRIM | ID: wpr-929194

ABSTRACT

Cardiovascular diseases account for approximately 80% of deaths among individuals with diabetes mellitus, with diabetic cardiomyopathy as the major diabetic cardiovascular complication. Hyperglycemia is a symptom that abnormally activates multiple downstream pathways and contributes to cardiac hypertrophy, fibrosis, apoptosis, and other pathophysiological changes. Although glycemic control has long been at the center of diabetes therapy, multicenter randomized clinical studies have revealed that intensive glycemic control fails to reduce heart failure-associated hospitalization and mortality in patients with diabetes. This finding indicates that hyperglycemic stress persists in the cardiovascular system of patients with diabetes even if blood glucose level is tightly controlled to the normal level. This process is now referred to as hyperglycemic memory (HGM) phenomenon. We briefly reviewed herein the current advances that have been achieved in research on the underlying mechanisms of HGM in diabetic cardiomyopathy.


Subject(s)
Humans , Cardiovascular Diseases , Diabetes Complications , Diabetes Mellitus , Diabetic Cardiomyopathies/etiology , Hyperglycemia/metabolism , Multicenter Studies as Topic
2.
Acta Physiologica Sinica ; (6): 461-468, 2022.
Article in Chinese | WPRIM | ID: wpr-939580

ABSTRACT

Histone methylation is one of the key post-translational modifications that plays a critical role in various heart diseases, including diabetic cardiomyopathy. A great deal of evidence has shown that histone methylation is closely related to hyperglycemia, insulin resistance, lipid and advanced glycation end products deposition, inflammatory and oxidative stress, endoplasmic reticulum stress and cell apoptosis, and these pathological factors play an important role in the pathogenesis of diabetic cardiomyopathy. In order to provide a novel theoretical basis and potential targets for the treatment of diabetic cardiomyopathy from the perspective of epigenetics, this review discussed and elucidated the association between histone methylation and the pathogenesis of diabetic cardiomyopathy in details.


Subject(s)
Humans , Diabetes Mellitus , Diabetic Cardiomyopathies/pathology , Histones , Methylation , Oxidative Stress , Protein Processing, Post-Translational
3.
Chinese Journal of Cardiology ; (12): 501-508, 2022.
Article in Chinese | WPRIM | ID: wpr-935176

ABSTRACT

Objective: To identify the differentially expressed circular RNA (circRNA) in the myocardium of diabetic cardiomyopathy (DCM) mice, and analyze their possible biological functions and related regulatory network. Methods: C57BL/6 mice, aged 8 weeks, and weighing were 21-27 g. Eight mice were selected as the control group and 15 mice were selected as the experimental group. The diabetic mice model was established by intraperitoneal injection of streptozotocin in the experimental group. One week after injection, the fasting blood glucose level of mice was measured, and 12 diabetic mice were included in the final experimental group. All mice were fed for 12 weeks under the same laboratory conditions. The cardiac structure and function were detected by echocardiography. Diabetic mice with the left ventricular ejection fraction less than 60% and the E/A less than 1.6 were selected as DCM group (n=3). Mice in DCM group and control group were then sacrificed under deep anesthesia. RNA was extracted from myocardial tissue. High-throughput RNA sequencing technology was used to sequence and identify the RNA in the myocardial tissue of DCM group and normal control group, and the difference was analyzed by DeSeq2. The analysis results were verified at the tissue level by RT-qPCR, and the differential circRNA were analyzed by GO and KEGG pathway analysis. The differentially expressed circRNA-microRNA(miRNA) interaction was predicted by the miRNA target gene prediction software. Results: A total of 63 differentially expressed circRNAs were found in the myocardium of DCM mice. The results of RT-qPCR showed that the tissue level expression of 8 differentially expressed circRNAs was consistent with the sequencing results, of which 7 were up-regulated and 1 was down-regulated. KEGG pathway analysis showed that the up-regulated circRNAs was mainly related to AMPK signal pathway and intercellular adhesion junction pathway, and the down-regulated circRNA was mainly related to cardiomyopathy. Go analysis showed that the up-regulated circRNA was mainly related to the binding process of ions, proteins, kinases and other factors in terms of molecular function, and was involved in regulating the intracellular structure, especially the composition of organelles in terms of cell components. The functional analysis of molecular function and cell components showed that the up-regulated circRNA were related to the cell component origin, recruitment and tissue, and thus participated in the regulation of cell biological process. The down regulated circRNA was related to catalytic activity in terms of molecular function, protein kinase binding process, transferase and calmodulin activity, and was closely related to the components of contractile fibers and the composition of myofibrils. These differentially expressed circRNAs were also related to biological processes such as lysine peptide modification, sarcomere composition, myofibril assembly, morphological development of myocardial tissue, myocardial hypertrophy and so on. Conclusions: In this study, we detected the novel differentially expressed circRNAs in the myocardium of DCM mice, and bioinformatics analysis confirmed that these circRNAs are related to oxidative stress, fibrosis and death of cardiomyocytes, and finally participate in the pathophysiological process of DCM.


Subject(s)
Animals , Mice , Diabetes Mellitus, Experimental , Diabetic Cardiomyopathies/genetics , Gene Expression Profiling/methods , Mice, Inbred C57BL , MicroRNAs/genetics , Myocardium , RNA, Circular , Stroke Volume , Ventricular Function, Left
4.
Braz. J. Pharm. Sci. (Online) ; 58: e19652, 2022. tab, graf
Article in English | LILACS | ID: biblio-1384005

ABSTRACT

Abstract Background and aim: Stingless bee propolis, a resinous compound processed by mandibular secretion of stingless bees, is used for maintenance of hygiene and stability of beehives. Research on stingless bee propolis shows therapeutic properties attributed to polyphenols exhibiting antioxidative, antihyperglycemic and antiischemic effect. However, the cardioprotective effect of stingless bee propolis on diabetic cardiomyopathy is unknown. Methods: Adult male Sprague Dawley rats were randomised to five groups: normal group, diabetic group, diabetic given metformin (DM+M), diabetic given propolis (DM+P) and diabetic given combination therapy (DM+M+P) and treated for four weeks. Body weight, fasting blood glucose, food and water intake were taken weekly. At the end of experiment, biomarkers of oxidative damage were measured in serum and heart tissue. Antioxidants in heart tissue were quantified. Part of left ventricle of heart was processed for histological staining including Haematoxylin and Eosin (H&E) stain for myocyte size and Masson's Trichrome (MT) stain for heart fibrosis and perivascular fibrosis. Results: Propolis alleviated features of diabetic cardiomyopathy such as myocyte hypertrophy, heart fibrosis and perivascular fibrosis associated with improvement in antioxidative status. Conclusion: This study reports beneficial effect of propolis and combination with metformin in alleviating histopathological feature of diabetic cardiomyopathy by modulating antioxidants, making propolis an emerging complementary therapy.


Subject(s)
Animals , Male , Rats , Propolis/adverse effects , Bees/classification , Diabetic Cardiomyopathies/pathology , Staining and Labeling/instrumentation , Blood Glucose/metabolism , Rats, Sprague-Dawley/classification , Cardiomegaly/pathology , Eosine Yellowish-(YS) , Drinking , Heart Ventricles/abnormalities , Hypoglycemic Agents , Metformin/agonists , Antioxidants/adverse effects
5.
ABC., imagem cardiovasc ; 35(2): eabc293, 2022. ilus, tab
Article in Portuguese | LILACS | ID: biblio-1400580

ABSTRACT

Fundamento: A ecocardiografia avançada com utilização de strain miocárdico bi e tridimensional propõe identificar a disfunção sistólica subclínica em diversas condições clínicas. No diabetes mellitus, seu papel é de grande interesse para diagnóstico precoce de cardiomiopatia diabética. Contudo, há grande heterogeneidade nos artigos publicados. Objetivo: Realizar uma revisão sistemática, para avaliar o papel atual da avaliação com strain nos pacientes com diabetes mellitus. Métodos: Após revisão sistemática em cinco bancos de dados, 19 estudos que utilizaram strain bidimensional e oito estudos que utilizaram strain tridimensional foram incluídos. Resultados:Na avaliação por strain bidimensional, a amostra totalizou 1.774 indivíduos com diabetes mellitus, com idade média de 57,1 anos e mediana de 55 anos, com equilíbrio em relação ao sexo dos participantes (47,5% do sexo feminino). Nos estudos que utilizaram strain tridimensional, foram incluídos 488 indivíduos com diabetes, com idade média de 55,7 anos e mediana de 63 anos, também com equilíbrio entre o sexo dos pacientes (51% do sexo feminino). O strain global longitudinal foi o marcador de deformação miocárdica que mais frequentemente conseguiu demonstrar diferença entre grupos com indivíduos diabéticos e controles. Conclusão: O strain miocárdico por speckle tracking bi e tridimensional permite identificar disfunção sistólica subclínica em pacientes diabéticos, o que se torna mais marcante nos pacientes com mais fatores de risco associados e com remodelamento ventricular.(AU)


Background: Advanced echocardiography using two- and three-dimensional myocardial strain proposes to identify subclinical systolic dysfunction in different clinical conditions. Strain assessment plays an important role in the early diagnosis of diabetic cardiomyopathy in diabetes mellitus (DM). However, the findings of published articles are heterogeneous. Here we conducted a systematic review to analyze the current role of strain assessment in patients with DM. Methods: This systematic review of five databases identified 19 studies that used twodimensional strain and 8 studies that used three-dimensional strain. Results: The studies of two-dimensional strain included 1,774 DM patients (mean age, 57.1 years; median age, 55 years; 47.5% women), while those of three-dimensional strain included 488 DM patients (mean age, 55.7 years; median age, 63 years; 51% women). Global longitudinal strain was the myocardial deformation marker that differed most frequently between the DM and control groups. Conclusion: Myocardial strain imaging by two- and three-dimensional speckle tracking echocardiography allows the identification of subclinical systolic dysfunction in DM patients, and differences become more marked when associated with risk factors and ventricular remodeling.(AU)


Subject(s)
Humans , Male , Female , Middle Aged , Echocardiography/methods , Diabetes Mellitus/physiopathology , Diabetic Cardiomyopathies/diagnosis , Diabetic Cardiomyopathies/prevention & control , Magnetic Resonance Spectroscopy/methods , Ventricular Dysfunction, Left/complications , Echocardiography, Three-Dimensional/methods , Heart Failure/mortality , Heart Injuries/prevention & control
6.
ABCS health sci ; 46: e021307, 09 fev. 2021. ilus, tab
Article in English | LILACS | ID: biblio-1349413

ABSTRACT

Diabetes mellitus (DM) is considered a 21st century pandemic and is often associated with cardiovascular disease (CVD). The aim of this integrative review was to analyze the cardioprotective effects of phosdodiesterase-5 (PDE5i) inhibitors in experimental diabetes models. The articles were selected from the PubMed, SciELO and LILACS databases from 2014 to 2019. The following descriptors were used in combination with the Boolean operators: Diabetes mellitus experimental AND Phosphodiesterase 5 inhibitors; Diabetic cardiomyopathies AND Phosphodiesterase 5 inhibitors. An initial sample of 155 articles was obtained, of which six met the criteria for the synthesis of the review. The studies analyzed showed that treatment with PDE5i in experimental models, resulted in positive effects on cardiac function and metabolic parameters. Similar results have also been seen in humans. The reduction in cardiac hypertrophy, apoptosis of cardiomyocytes, pro-inflammatory factors and oxidative stress and the modulation of transcription factors involved in diabetes homeostasis, were prevalent among studies. The mechanisms of action involved in cardioprotection have not yet been fully elucidated, however the restoration of the activated cyclic guanosine monofate (cGMP) pathway by soluble guanylate cyclase (sGC) via nitric oxide (NO) was a common mechanism among the studies.


O Diabetes mellitus (DM) é considerado uma pandemia do século XXI e está frequentemente associado às doenças cardiovasculares (DCVs). O objetivo desta revisão integrativa foi analisar os efeitos cardioprotetores de inibidores da fosdodiesterase 5 (PDE5i) em modelos de diabetes experimental. Os artigos foram selecionados nas bases de dados PubMed, SciElo e LILACS no período de 2014 a 2019. Foram utilizados os seguintes descritores combinados com os operadores booleanos: Diabetes mellitus experimental AND Phosphodiesterase 5 inhibitors; Diabetic cardiomyopathies AND Phosphodiesterase 5 inhibitors. Foi obtida uma amostra inicial de 155 artigos, dos quais seis se enquadraram nos critérios para a síntese da revisão. Os estudos analisados evidenciaram que o tratamento com os PDEi5 em modelos experimentais, resultou em efeitos positivos sobre a função cardíaca e parâmetros metabólicos. Resultados semelhantes também foram observados em humanos. A redução da hipertrofia cardíaca, apoptose de cardiomiócitos, fatores pró-inflamatórios e estresse oxidativo e a modulação de fatores de transcrição envolvidos na homeostasia do diabetes, foram achados prevalentes entre os estudos. Os mecanismos de ação envolvidos na cardioproteção ainda não foram totalmente elucidados, contudo a restauração da via da guanosina monofato cíclica ativada (GMPc) pela Guanilato ciclase solúvel (GCs) via Óxido Nítrico (NO) foi um mecanismo comum entre os estudos.


Subject(s)
Humans , Diabetes Mellitus, Experimental , Diabetic Cardiomyopathies , Phosphodiesterase 5 Inhibitors , Noncommunicable Diseases
7.
Article in Chinese | WPRIM | ID: wpr-879143

ABSTRACT

Pharmacology network was used to investigate the common key target and signaling pathway of Notoginseng Radix et Rhizoma in the protection against diabetic nephropathy(DN), diabetic encephalopathy(DE) and diabetic cardiomyopathy(DCM). The chemical components of Notoginseng Radix et Rhizoma were obtained through TCMSP database and literature mining, and SwissTargetPrediction database was used to predict potential targets of Notoginseng Radix et Rhizoma. The disease targets of DN, DE and DCM were obtained through OMIM and GeneCards databases. The overlapped targets of component targets and disease targets of DN, DE and DCM were obtained, and the network of "chemical component-target-disease" was established. The enriched GO and KEGG of the overlapped genes were investigated by using ClueGo plug-in with Cytoscape. At the same time, the PPI network was constructed through STRING database, and the common key targets for the treatment of three diseases by Notoginseng Radix et Rhizoma were obtained through topological parametric mathematical analysis by Cytoscape. A total of 166 chemical components and 835 component targets were screened out from Notoginseng Radix et Rhizoma. Briefly, 216, 194 and 230 disease targets of DN, DE and DCM were collected, respectively. And 54, 45 and 57 overlapped targets were identified when overlapping these disease targets with component targets of Notoginseng Radix et Rhizoma, respectively. Enrichment analysis indicated that the AGE-RAGE signaling pathway and FoxO signaling pathway were the common pathways in the protection of Notoginseng Radix et Rhizoma against DN, DE and DCM. Network analysis of the overlapped targets showed that TNF, STAT3, IL6, VEGFA, MAPK8, CASP3 and SIRT1 were identified as key targets of Notoginseng Radix et Rhizoma against DN, DE and DCM, the selected key targets were verified by literature review, and it was found that TNF, IL6, VEGFA, CASP3 and SIRT1 had been reported in the literature. In addition, there were the most compounds corresponding to the commom core target STAT3, indicating that more compounds in Notoginseng Radix et Rhizoma could regulate STAT3. This study indicated that Notoginseng Radix et Rhizoma potentially protected against DN, DE and DCM through regulating AGE-RAGE signaling pathway and FoxO signaling pathway and 7 common targets including TNF, STAT3, IL6, VEGFA, MAPK8, CASP3 and SIRT1. This study provided a reference for the research of "different diseases with same treatment" and also elucidated the potential mechanism of Notoginseng Radix et Rhizoma against DN, DE and DCM.


Subject(s)
Humans , Brain Diseases , Diabetes Mellitus , Diabetic Cardiomyopathies/genetics , Diabetic Nephropathies/genetics , Research Design , Signal Transduction
8.
Clinics ; 76: e2669, 2021. graf
Article in English | LILACS | ID: biblio-1278915

ABSTRACT

OBJECTIVES: This study aimed to explore the efficacy of combination treatment with dendrobium mixture and metformin (Met) in diabetic cardiomyopathy (DCM) and its effects on NEAT1 and the Nrf2 signaling pathway. METHODS: H9c2 cells were maintained in medium supplemented with either low (5.5 mmol/L) or high (50 mmol/L) glucose. Male Sprague-Dawley rats were fed a high-glucose diet and administered a single, low dose of streptozotocin (35 mg/kg) via intraperitoneal injection to induce the development of DM. After induction of DM, the rats were treated with dendrobium mixture (10 g/kg) and Met (0.18 g/kg) daily for 4 weeks. Next, quantitative reverse transcription (qRT)-PCR and western blotting were performed to evaluate the expression levels of target genes and proteins. Flow cytometry was performed to assess apoptosis, and hematoxylin and eosin staining was performed to evaluate the morphological changes in rat cardiac tissue. RESULTS: In patients with diabetes mellitus (DM) and myocardial cells and heart tissues from rats with high glucose-induced DM, NEAT1 was downregulated, and the expression levels of Nrf2 were decreased (p<0.01, p<0.001). The combination of dendrobium mixture and Met upregulated the expression of NEAT1 which upregulated Nrf2 by targeting miR-23a-3p, resulting in reduced apoptosis and improved cardiac tissue morphology (p<0.01, p<0.001). CONCLUSION: Dendrobium mixture and Met upregulated the expression of NEAT1 in DCM, thereby inhibiting apoptosis of myocardial cells.


Subject(s)
Humans , Animals , Male , Rats , Dendrobium , MicroRNAs , Diabetes Mellitus , Diabetic Cardiomyopathies/genetics , Diabetic Cardiomyopathies/drug therapy , Metformin , Apoptosis , RNA, Long Noncoding/genetics
9.
Rev. Soc. Argent. Diabetes ; 54(supl. 2): 91-106, mayo - ago. 2020. tab
Article in Spanish | LILACS, BINACIS | ID: biblio-1122959

ABSTRACT

Desde que el estudio Framingham en 1974 reportó un aumento de dos a cinco veces en el riesgo de desarrollar insuficiencia cardíaca (IC) en pacientes con diabetes mellitus (DM), otros estudios observacionales confirmaron esta asociación que ha tomado gran visibilidad en los últimos años a partir de los resultados de los estudios de seguridad cardiovascular de las drogas antidiabéticas. La IC se define como un síndrome clínico que resulta del deterioro funcional o estructural del llenado ventricular o la eyección de sangre. Puede clasificarse según la fracción de eyección, la presencia de síntomas y la limitación de la actividad física. Existen distintos factores asociados a la IC en personas con DM como la edad, la antigüedad de la enfermedad, la utilización de insulina, la enfermedad coronaria, la hipertensión arterial, la enfermedad arterial periférica, el aumento de creatinina, el escaso control glucémico, la albuminuria y la obesidad. A su vez la IC se asocia a insulinorresistencia y a estados disglucémicos que se consideran de riesgo para el desarrollo de DM. En la fisiopatología están implicados el sistema nervioso simpático, el sistema renina angiotensina aldosterona, los péptidos natriuréticos, alteraciones renales, remodelación del ventrículo izquierdo, miocardiopatía diabética, neuropatía autonómica cardíaca y la inflamación. El diagnóstico de IC es clínico; los estudios complementarios orientan en el diagnóstico etiológico y son útiles en el seguimiento. El buen control glucémico es importante pero no suficiente para reducir el desarrollo de IC. Se ha descripto que algunos antidiabéticos podrían incrementar el riesgo de falla cardíaca y, por el contrario, otros tendrían un efecto beneficioso. El tratamiento de la IC no difiere de una persona sin DM. Dado que el pronóstico de la IC en los pacientes con DM es más severo, los esfuerzos deben centrarse en prevenir, diagnosticar y tratar los factores de riesgo cardiovascular para reducir el desarrollo de IC.


Since the Framingham study in 1974 reported a 2 to 5 fold increase in the risk of developing heart failure (HF) in patients with diabetes mellitus (DM), other observational studies confirmed this association that has gained great visibility in recent years from of the results of cardiovascular safety studies of antidiabetic drugs. HF is defined as a clinical syndrome that results from functional or structural deterioration of ventricular filling or blood ejection. It can be classified according to the ejection fraction, the presence of symptoms and the limitation to physical activity. There are different factors associated with HF in people with DM such as age, duration of the disease, insulin use, coronary heart disease, high blood pressure, peripheral arterial disease, increased creatinine, poor glycemic control, albuminuria and obesity. In turn, HF is associated with insulin resistance and dysglycemic states that are considered of risk for the development of DM. Pathophysiology involves the sympathetic nervous system, the renin angiotensin aldosterone system, natriuretic peptides, kidney abnormalities, left ventricular remodeling, diabetic cardiomyopathy, autonomic cardiac neuropathy, and inflammation. The diagnosis of HF is clinical, complementary studies guide the etiological diagnosis and are useful for follow-up. Good glycemic control is important but not sufficient to reduce the development of HF. It has been described that some antidiabetics could increase the risk of heart failure, while others would have a beneficial effect. The treatment of HF does not differ from a person without DM. Since the prognosis of HF in patients with DM is more severe, efforts should be focused on preventing, diagnosing and treating cardiovascular risk factors, to reduce the development of HF


Subject(s)
Humans , Diabetes Mellitus, Type 2 , Therapeutics , Coronary Disease , Diabetic Cardiomyopathies , Heart Failure
10.
Article in English | WPRIM | ID: wpr-811149

ABSTRACT

No abstract available.


Subject(s)
Diabetic Cardiomyopathies , MicroRNAs
11.
Rev. Assoc. Med. Bras. (1992, Impr.) ; 65(1): 61-69, Jan. 2019. tab, graf
Article in English | LILACS | ID: biblio-985004

ABSTRACT

SUMMARY Although long ago described, there is no established consensus regarding the real existence of Diabetic Cardiomyopathy (CMPDM). Due to its complex pathophysiology, it has been difficult for clinical and experimental research to establish clear connections between diabetes mellitus (DM) and heart failure (HF), as well as to solve the mechanisms of the underlying myocardial disease. However, the epidemiological evidence of the relationship of these conditions is undisputed. The interest in understanding this disease has intensified due to the recent results of clinical trials evaluating new glucose-lowering drugs, such as sodium-glucose transporter inhibitors 2, which demonstrated favorable responses considering the prevention and treatment of HF in patients with DM. In this review we cover aspects of the epidemiology of CMPDM and its possible pathogenic mechanisms, as well as, present the main cardiac phenotypes of CMPDM (HF with preserved and reduced ejection fraction) and implications of the therapeutic management of this disease.


RESUMO Apesar de há muito tempo descrita, não existe consenso estabelecido quanto à real existência da cardiomiopatia diabética (CMPDM). Devido à sua complexa fisiopatologia, tem sido árduo à pesquisa clínica e experimental estabelecer conexões claras entre diabetes mellitus (DM) e insuficiência cardíaca (IC), assim como solucionar os mecanismos da doença subjacente do miocárdio. No entanto, as evidências epidemiológicas da relação dessas condições são incontestáveis. O interesse em compreender melhor essa doença tem recrudescido devido aos recentes resultados de ensaios clínicos avaliando novos fármacos hipoglicemiantes, como os inibidores do transportador de sódio-glicose 2, que demonstraram respostas favoráveis, considerando-se a prevenção e tratamento da IC em pacientes portadores de DM. Nesta revisão, percorremos aspectos da epidemiologia da CMPDM e de seus possíveis mecanismos patogênicos, além de apresentarmos os principais fenótipos cardíacos da CMPDM (IC com fração de ejeção preservada e reduzida) e implicações do manejo terapêutico desta doença.


Subject(s)
Humans , Diabetic Cardiomyopathies/diagnostic imaging , Phenotype , Echocardiography , Risk Factors , Evidence-Based Medicine , Diabetic Cardiomyopathies/therapy , Diabetic Cardiomyopathies/epidemiology
12.
Article in English | WPRIM | ID: wpr-765654

ABSTRACT

Diabetes mellitus increases the risk for the development of heart failure even in the absence of coronary artery disease and hypertension, a cardiac entity termed diabetic cardiomyopathy (DC). Clinically, DC is increasingly recognized and typically characterized by concentric cardiac hypertrophy and diastolic dysfunction, ultimately resulting in heart failure with preserved ejection fraction (HFpEF) and potentially even heart failure with reduced ejection fraction (HFrEF). Numerous molecular mechanisms have been proposed to underlie the alterations in myocardial structure and function in DC, many of which show similar alterations in the failing heart. Well investigated and established mechanisms of DC include increased myocardial fibrosis, enhanced apoptosis, oxidative stress, impaired intracellular calcium handling, substrate metabolic alterations, and inflammation, among others. In addition, a number of novel mechanisms that receive increasing attention have been identified in recent years, including autophagy, dysregulation of microRNAs, epigenetic mechanisms, and alterations in mitochondrial protein acetylation, dynamics and quality control. This review aims to provide an overview and update of established underlying mechanisms of DC, as well as a discussion of recently identified and emerging mechanisms that may also contribute to the structural and functional alterations in DC.


Subject(s)
Acetylation , Apoptosis , Autophagy , Calcium , Cardiomegaly , Coronary Artery Disease , Diabetes Mellitus , Diabetic Cardiomyopathies , Epigenomics , Fibrosis , Heart , Heart Failure , Hypertension , Inflammation , MicroRNAs , Mitochondrial Proteins , Oxidative Stress , Quality Control
13.
Article in Korean | WPRIM | ID: wpr-761473

ABSTRACT

There is a close relationship between diabetes mellitus and heart failure, both of which are known to increase morbidity and mortality. Diabetes can cause or aggravate heart failure, and heart failure can precipitate diabetes. Diabetes mellitus causes structural and functional changes in the heart, such as fibrosis of the myocardium and left ventricular dysfunction. The mechanisms of diabetic cardiomyopathy are metabolic disturbance, myocardial fibrosis, microvascular disease, and autonomic dysfunction. Improper blood glucose control leads to deterioration of heart failure, but the role of strict glycemic control in reducing heart failure is unclear. The role of SGLT2 inhibitors in reducing the incidence of heart failure is of great importance in the treatment of diabetic patients. However, further long-term follow-up and safety studies are needed.


Subject(s)
Humans , Blood Glucose , Diabetes Complications , Diabetes Mellitus , Diabetic Cardiomyopathies , Fibrosis , Follow-Up Studies , Heart Failure , Heart , Incidence , Mortality , Myocardium , Ventricular Dysfunction, Left
14.
Article in Chinese | WPRIM | ID: wpr-1008379

ABSTRACT

Diabetic cardiomyopathy( DCM) is one of the major cardiovascular complications of diabetes mellitus. Based on the clinical efficacy of Danzhi Jiangtang Capsules( DJC) in the prevention and treatment of diabetes and its cardiovascular complications,both in vivo and in vitro methods were adopted to investigate its effect and underlying mechanism of protecting myocardial injury induced by diabetes. The type 2 diabetic rats were prepared by feeding high-energy food combined with streptozotin( STZ) injection,and the effects of DJC were observed by blood sugar,blood lipid,hemodynamic index,cardiac weight index and the change of cardiac pathological morphology. The protein expressions of TLR4,MyD88 and NF-κB p65 in myocardial tissue were detected and the possible mechanism was preliminarily analyzed. Besides this,DJC containing serum was prepared,H9 c2 cardiomyocyte induced by high sugar were studied to investigate the mechanism of TLR4/MyD88/NF-κB signaling pathway regulating cardiomyocyte injury and the therapeutic effect of DJC. The results demonstrated that fasting blood sugar,glycosylated hemoglobin,total cholesterol and glycerol triglyceride were significantly reduced( P<0. 01,P<0. 05). Cardiac weight index,left ventricle weight index,LVEDP and the protein expressions of TLR4,MyD88 and NF-κB p65 were significantly reduced( P<0. 01,P<0. 05). LVSP,+dp/dtmaxand-dp/dtmaxincreased significantly( P<0. 01,P< 0. 05). Moreover,the pathological damage of myocardial tissue in rats improved significantly. Meanwhile,the protein expressions of TLR4,MyD88 and NF-κB p65 in cardiomyocytes induced by high sugar were significantly inhibited( P<0. 01).It showed that DJC were effective in preventing and treating myocardial injury induced by diabetes and its mechanism may be related to the over-expression of TLR4/MyD88/NF-κB signaling pathway induced by high sugar.


Subject(s)
Animals , Rats , Blood Glucose , Capsules , Diabetes Mellitus, Experimental/complications , Diabetic Cardiomyopathies/drug therapy , Drugs, Chinese Herbal/therapeutic use , Myeloid Differentiation Factor 88/metabolism , NF-kappa B/metabolism , Rats, Sprague-Dawley , Signal Transduction , Toll-Like Receptor 4/metabolism
15.
Rev. colomb. cardiol ; 25(1): 51-54, ene.-feb. 2018. tab
Article in Spanish | LILACS, COLNAL | ID: biblio-959945

ABSTRACT

Resumen Objetivo: Estimar la prevalencia de pacientes con probable miocardiopatía diabética (sin exigir biopsia endomiocárdica), analizando sus características y comparándolas con pacientes no diabéticos con insuficiencia cardiaca idiopática. Métodos: Estudio retrospectivo sobre una cohorte de 270 pacientes que ingresaron de manera consecutiva por insuficiencia cardiaca. De estos se excluyeron del estudio todos aquellos que tuvieran una causa conocida de insuficiencia cardiaca (cardiopatía isquémica, hipertensiva, hipertrófica, valvular u otras). En total 58 pacientes, 18 de los cuales eran diabéticos (la causa de la insuficiencia cardiaca pudo ser la miocardiopatía diabética) y 40 sin diabetes (insuficiencia cardiaca idiopática). Se procedió a comparar las características entre ambos grupos. El análisis estadístico y la comparación de las distintas variables se realizó mediante el programa SPSS versión 20.0. Resultados: De 270 pacientes estudiados, 18 podrían haber sido diagnosticados con miocardiopatía diabética, lo que supone hasta un 6% de la insuficiencia cardiaca en esta serie. Conclusiones: Se considera que este estudio puede hacer reflexionar sobre la prevalencia global de la miocardiopatía diabética, sus características y sus dificultades diagnósticas.


Abstract Objective: To determine the prevalence of patients with probable diabetic cardiomyopathy (without requesting an endomyocardial biopsy), as well as to analyse its characteristics and comparing them with non-diabetic patients with idiopathic heart failure. Methods: A retrospective study was conducted on a cohort of 270 patients consecutively admitted to hospital due to heart failure. Excluded from the study were those who had a known cause of heart failure (ischaemic, hypertensive, hypertrophic, valvular, or other causes of heart disease). This left a total of 58 patients, 18 of whom were diabetics (the cause of heart failure could be due to diabetic cardiomyopathy) and 40 non-diabetics (idiopathic heart failure). A comparison was made between the characteristics of both groups. The statistical analysis and the comparison of the different variables were performed using Version 20.0 of the SPSS program. Results: Of the 270 patients studied, 18 could have been diagnosed with diabetic cardiomyopathy, which would be 6% of the cardiac failures in this series. Conclusions: It is believed that this study can lead to reflecting on the overall prevalence of diabetic cardiomyopathy, its characteristics, and the difficulties in its diagnosis.


Subject(s)
Humans , Male , Female , Diabetes Mellitus , Heart Failure , Myocardial Ischemia , Diabetic Cardiomyopathies , Cardiomyopathies
16.
Article in Chinese | WPRIM | ID: wpr-776430

ABSTRACT

Diabetic cardiomyopathy (DCM) is characterized by left ventricular hypertrophy, myocardial fibrosis and diastolic dysfunction, which are uncorrelated with underlying coronary artery disease or hypertension. As an important metabolic organelle, mitochondria directly involve the process of cell growth, proliferation, signal transduction, apoptosis and so on. Recent studies have demonstrated a close correlation between the mitochondrial dysfunction and the pathogenesis of diabetic cardiomyopathy. The underlying effects of mitochondrial dysfunction in the progress of diabetic cardiomyopathy involve disturbed metabolism, oxidative stress, defective calcium handling, mitochondrial uncoupling, apoptosis, imbalance of mitochondrial quality control and regulation of MicroRNAs. Traditional Chinese medicines have been widely applied in clinic. Nowadays, more and more herbs of extracts of traditional Chinese medicines have been proved to ameliorate diabetic myocardial injury. Because the improvement of mitochondrial dysfunction has emerged as a promising therapeutic strategy, this review summarizes these effects of mitochondrial dysfunction in diabetic cardiomyopathy, and discusses the intervention studies of traditional Chinese medicine in the field, in expectation to provide new ideas for DCM prevention and treatment.


Subject(s)
Humans , Diabetic Cardiomyopathies , Drug Therapy , Pathology , Drugs, Chinese Herbal , Therapeutic Uses , Medicine, Chinese Traditional , Mitochondria , Pathology , Myocardium
17.
Article in English | WPRIM | ID: wpr-772782

ABSTRACT

OBJECTIVE@#To investigate the effect of tea polyphenols on cardiac function in rats with diabetic cardiomyopathy, and the mechanism by which tea polyphenols regulate autophagy in diabetic cardiomyopathy.@*METHODS@#Sixty Sprague-Dawley (SD) rats were randomly divided into six groups: a normal control group (NC), an obesity group (OB), a diabetic cardiomyopathy group (DCM), a tea polyphenol group (TP), an obesity tea polyphenol treatment group (OB-TP), and a diabetic cardiomyopathy tea polyphenol treatment group (DCM-TP). After successful modeling, serum glucose, cholesterol, and triglyceride levels were determined; cardiac structure and function were inspected by ultrasonic cardiography; myocardial pathology was examined by staining with hematoxylin-eosin; transmission electron microscopy was used to observe the morphology and quantity of autophagosomes; and expression levels of autophagy-related proteins LC3-II, SQSTM1/p62, and Beclin-1 were determined by Western blotting.@*RESULTS@#Compared to the NC group, the OB group had normal blood glucose and a high level of blood lipids; both blood glucose and lipids were increased in the DCM group; ultrasonic cardiograms showed that the fraction shortening was reduced in the DCM group. However, these were improved significantly in the DCM-TP group. Hematoxylin-eosin staining showed disordered cardiomyocytes and hypertrophy in the DCM group; however, no differences were found among the remaining groups. Transmission electron microscopy revealed that the numbers of autophagosomes in the DCM and OB-TP groups were obviously increased compared to the NC and OB groups; the number of autophagosomes in the DCM-TP group was reduced. Western blotting showed that the expression of LC3-II/I and Beclin-1 increased obviously, whereas the expression of SQSTM1/p62 was decreased in the DCM and OB-TP groups (P<0.05).@*CONCLUSIONS@#Tea polyphenols had an effect on diabetic cardiomyopathy in rat cardiac function and may alter the levels of autophagy to improve glucose and lipid metabolism in diabetes.


Subject(s)
Animals , Male , Rats , Autophagy , Beclin-1 , Blood Glucose , Body Weight , Diabetic Cardiomyopathies , Drug Therapy , Pathology , Lipids , Blood , Myocardium , Pathology , Polyphenols , Pharmacology , Rats, Sprague-Dawley , Tea , Chemistry
18.
Article in Chinese | WPRIM | ID: wpr-771695

ABSTRACT

To explore the protective effect of naringin(Nar) on the injury of myocardium tissues induced by streptozotocin(STZ) in diabetic rats and the relationship with oxidative stress and endoplasmic reticulum stress(ERS), the male SD rats were intraperitoneally injected with streptozotocin(STZ, 60 mg·kg⁻¹) to establish the diabetic rat model and then randomly divided into the type 1 diabetic rat group(T1DR), the low-dose Nar group(Nar25), the middle-dose Nar group(Nar50) and the high-dose Nar group(Nar100). The normal rats were designed as control group(Con). Nar25, Nar50, Nar100 groups were orally administered with Nar at the doses of 25.0, 50.0, 100.0 mg·kg⁻¹ per day, respectively, while the normal group and the T1DR group were orally administered with saline. At the 8th week after treatment, fasting plasma glucose and heart mass index were measured. The pathological changes in myocardial tissues were observed by microscope. The cardiac malondialdehyde(MDA) level and superoxide dismutase(SOD) activities were measured. The gene and protein expressions of glucose-regulated protein 78(GRP78), C/EBP homologous protein(CHOP), cysteinyl aspartate-specific proteinase 12(caspase 12) were detected by qRT-PCR and Western blot. According to the results, compared with control group, the myocardial structure was damaged, the content of MDA was increased, while the activities of SOD were decreased(<0.05) in T1DR group. GRP78, CHOP and caspase 12 mRNA and protein expressions were increased significantly in T1DR group(<0.05, <0.01). Compared with T1DR group, myocardial structure damage was alleviated in Nar treatment group. The content of MDA was decreased, while the activities of SOD were increased significantly. The mRNA and protein expressions of GRP78, CHOP and caspase 12 were increased, especially in middle and high-dose groups(<0.05, <0.01). After treatment with Nar for 8 weeks, myocardial structure damage was obviously alleviated in Nar treatment groups. The content of MDA was decreased, while the activities of SOD were increased significantly in myocardial tissues. The mRNA and protein expressions of GRP78, CHOP and caspase 12 were increased, especially in middle and high-dose groups(<0.05, <0.01). The findings suggest that Nar may protect myocardium in diabetic rats by reducing mitochondrial oxidative stress injuries and inhibiting the ERS-mediated cell apoptosis pathway.


Subject(s)
Animals , Male , Rats , Apoptosis , Cardiotonic Agents , Pharmacology , Caspase 12 , Metabolism , Diabetes Mellitus, Experimental , Diabetic Cardiomyopathies , Drug Therapy , Endoplasmic Reticulum Stress , Flavanones , Pharmacology , Heat-Shock Proteins , Metabolism , Malondialdehyde , Metabolism , Oxidative Stress , Rats, Sprague-Dawley , Superoxide Dismutase , Metabolism , Transcription Factor CHOP , Metabolism
19.
Rev. urug. cardiol ; 32(3): 264-276, dic. 2017. tab
Article in Spanish | LILACS | ID: biblio-903594

ABSTRACT

La enfermedad coronaria, la hipertensión arterial y la diabetes son factores de riesgo independientes para el desarrollo de insuficiencia cardíaca y muerte. La cardiomiopatía diabética (CMD) es una de las etiologías frecuentes de cardiopatía en pacientes con diabetes tipo 1 y tipo 2. Si bien se suele plantear la CMD como la causa de la cardiopatía cuando se excluyen la hipertensión arterial, las valvulopatías y la enfermedad arterial coronaria aterotrombótica, estas coexisten con frecuencia e incluso también con la neuropatía autónoma cardiovascular. En los pacientes con CMD se puede demostrar mediante tests serológicos y por imagen alteraciones a nivel molecular, metabólico, mitocondrial, celular y tisular con infiltración grasa del músculo cardíaco, vinculadas a hiperglicemia, hiperinsulinemia y resistencia a la insulina, así como a lipotoxicidad por ácidos grasos libres, que son responsables del desarrollo de la CMD. Esta entidad primero determina disfunción diastólica del ventrículo izquierdo, más tarde disfunción sistólica e insuficiencia cardíaca. Se diagnostica mediante estudios serológicos de marcadores biológicos múltiples y por técnicas de imagen que evidencian la disfunción ventricular y mejoran la predicción pronóstica de enfermedad cardiovascular en diabéticos. En base a dichas pruebas se ha propuesto una clasificación por estadios o fenotipos clínicos de la CMD, que apunta a su diagnóstico precoz. Puede ser asintomática o ser responsable de síntomas y manifestaciones severas tales como insuficiencia cardíaca, arritmias y muerte súbita. Se puede asociar a hipertensión arterial, a enfermedad coronaria, a otras manifestaciones de microangiopatía y macroangiopatía aterotrombótica y a mortalidad cardiovascular. La prevención y el tratamiento intensivo multifactorial y personalizado de la diabetes, de todas sus alteraciones metabólicas y de la cardiopatía, mejoran la calidad y prolongan la vida. Se espera que investigaciones recientes, en proceso y futuras, determinen portentosos avances en la prevención y en el tratamiento de la CMD, que constituye una de las serias amenazas a la salud de la humanidad.


Coronary heart disease, hypertension and diabetes mellitus are independent risk factors for heart failure and death. Diabetic cardiomyopathy (DCM) is one of the common etiologies of cardiac disease in patients with diabetes type 1 or 2. Although DCM is often considered as the cause of heart disease when arterial hypertension, valvulopathies and atherothrombotic coronary artery are excluded, they coexist frequently, as well as with cardiovascular neuropathy. In patients with DCM, serological and imaging tests can show alterations at the molecular, metabolic, mitochondrial, cellular and tissue levels with fatty infiltration of the heart muscle, linked to hyperglycemia, hyperinsulinemia, insulin resistance, and lipotoxicity by fatty free acids, which are responsible for the development of the cardiomyopathy. The DCM first determines left ventricular diastolic dysfunction, later systolic dysfunction and heart failure. It is diagnosed by serological tests of multiple biological markers and by imaging tests that demonstrate ventricular dysfunction and improve the prognostic prediction of cardiovascular disease in diabetics. Based on these tests, a classification by stages or clinical phenotypes of DCM, which aims at its early diagnosis, has been proposed. It can be asymptomatic or be responsible for symptoms and severe manifestations such as heart failure, arrhythmias and sudden death, and may associate hypertension, coronary disease, other manifestations of microangiopathy and atherothrombotic macroangiopathy and cardiovascular mortality. The prevention and intensive multifactorial and personalized treatment of diabetes and all its metabolic and cardiac alterations, improve quality and prolong life. It is expected that ongoing and future research will determine breakthroughs in the prevention and treatment of DCM, which is one of the serious threats to the health of mankind.


Subject(s)
Humans , Diabetes Mellitus, Type 2/complications , Diabetic Cardiomyopathies/diagnosis , Diabetic Cardiomyopathies/physiopathology , Diabetic Cardiomyopathies/therapy , Diagnostic Techniques and Procedures , Diabetes Mellitus, Type 1/complications
20.
Arch. cardiol. Méx ; 87(4): 278-285, oct.-dic. 2017. tab, graf
Article in English | LILACS | ID: biblio-887537

ABSTRACT

Abstract: Objectives: To establish a relationship between global longitudinal strain (GLS) and Galectin-3 in pre-clinical heart failure in diabetic patients. Galectin-3 is a biomarker in heart failure with depressed ejection fraction (HFdEF). The hypothesis is presented that Galectin-3 is related to GLS and can detect left ventricular dysfunction in heart failure with preserved ejection fraction. Methods: Galectin-3 and GLS were measured in 121 asymptomatic individuals: 14 diabetics with mild depressed ejection fraction (mdEF) (LVEF 47.0 ± 6.9); 76 diabetics with preserved ejection fraction (LVEF 61 ± 5.5), and 31 controls (61.7 ± 5.1). Results: Galectin-3 was elevated in all diabetics vs controls (3.46 ± 1.36 ng/ml vs 2.78 ± 0.91 ng/ml; p = .003). It was also elevated in mdEF (3.76 ± 1.12 ng/ml vs 2.78 ± 0.9 ng/ml; p = .009) and pEF subjects (3.41 ± 1.40 ng/ml vs 2.78 ± 0.9 ng/ml; p = .058), respectively, vs controls. No difference in Gal-3 was found between diabetic groups (p = .603). Diabetics had lower GLS than controls (-18.5 ± 3.9 vs -20 ± 2.6; p = .022). Diabetics with mdEF had lower GLS than those with pEF (-13.3 ± 3.41 vs -19 ± 3.2; P<.001). There was no difference in GLS with pEF compared to controls (-19.4 ± 3.2 vs -20 ± 2.6; p = .70). Conclusions: Galectin-3 is elevated in diabetic patients with mdEF, and is associated with a diminished GLS. GLS could be an early marker of left ventricular dysfunction as well as evidence of diabetic cardiomyopathy.


Resumen: Objetivos: Establecer una asociación entre deformación longitudinal global (DLG) y galectina-3 en insuficiencia cardiaca preclínica en pacientes diabéticos. Galectina-3 es un biomarcador en insuficiencia cardiaca con fracción de eyección deprimida. Nuestra hipótesis es que la DLG y galectina-3 correlacionan y pueden detectar disfunción ventricular en insuficiencia cardiaca con FEVI preservada. Métodos: Se midieron galectina-3 y DLG en 121 individuos asintomáticos: 14 diabéticos con FEVI deprimida leve (FEdl) (FEVI 47 ± 6.9); 76 diabéticos con FEVI preservada (FEp) (FEVI 61 ± 5.5) y 31 sujetos controles (FEVI 61.7 ± 5.1). Resultados: Galectina-3 se encontró elevada en todos los diabéticos vs controles (3.46 ± 1.36 ng/ml vs 2.78 ± 0.91 ng/ml; p = 0.003). Está elevada en sujetos con FEdl (3.76 ± 1.12 vs 2.78 ± 0.9 vs ng/ml p = 0.009) y FEp (3.41 ± 1.40 vs 2.78 ± 0.9 ng/ml p = 0.058), respectivamente vs controles; no encontramos diferencia en galectina-3 en ambos grupos de diabéticos (p = 0.603). Los diabéticos tienen menor DLG que los controles (-18.5 ± 3.9 vs -20 ± 2.6; p = 0.022). Los diabéticos con FEdl tienen DLG más disminuida que aquellos con FEp (-13.3 ± 3.41 vs -19 ± 3.2; p < 0.001). No existe diferencia en DLG con FEp y controles (-19.4 ± 3.2 vs -20 ± 2.6; p = 0.70). Conclusiones: Galectina-3 está elevada en diabéticos con FEdl y correlaciona DLG disminuida. DLG podría ser un marcador temprano de disfunción ventricular y evidencia en miocardiopatía diabética.


Subject(s)
Humans , Male , Female , Middle Aged , Stroke Volume , Galectin 3/blood , Diabetic Cardiomyopathies/physiopathology , Diabetic Cardiomyopathies/blood , Blood Proteins , Echocardiography , Biomarkers/blood , Galectins , Diabetic Cardiomyopathies/diagnostic imaging
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