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1.
Front Cardiovasc Med ; 11: 1287852, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38601040

RESUMO

The arterial circulatory system diseases are common in clinical practice, and their treatment options have been of great interest due to their high morbidity and mortality. Drug-eluting balloons, as a new type of endovascular interventional treatment option, can avoid the long-term implantation of metal stents and is a new type of angioplasty without stents, so drug-eluting balloons have better therapeutic effects in some arterial circulatory diseases and have been initially used in clinical practice. In this review, we first describe the development, process, and mechanism of drug-eluting balloons. Then we summarize the current studies on the application of drug-eluting balloons in coronary artery lesions, in-stent restenosis, and peripheral vascular disease. As well as the technical difficulties and complications in the application of drug-eluting balloons and possible management options, in order to provide ideas and help for future in-depth studies and provide new strategies for the treatment of more arterial system diseases.

2.
Front Immunol ; 14: 1213473, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-37809091

RESUMO

Diabetic kidney disease (DKD) is a chronic inflammatory condition that affects approximately 20-40% of individuals with diabetes. Sodium-glucose co-transporter 2 (SGLT-2) inhibitors, emerging as novel hypoglycemic agents, have demonstrated significant cardiorenal protective effects in patients with DKD. Initially, it was believed that the efficacy of SGLT-2 inhibitors declined as the estimated glomerular filtration rate (eGFR) decreased, which led to their preferential use in DKD patients at G1-G3 stages. However, recent findings from the DAPA-CKD and EMPA-KIDNEY studies have revealed equally beneficial cardiorenal effects of SGLT-2 inhibitors in individuals at stage G4 DKD, although the underlying mechanism behind this phenomenon remains unclear. In this comprehensive analysis, we provide a systematic review of the mechanisms and functioning of SGLT-2 inhibitors, potential renal protection mechanisms, and the therapeutic efficacy and safety of SGLT-2 inhibitors in kidney diseases, with a particular focus on stage G4 DKD. Gaining a deeper understanding of the renal protective effect of SGLT-2 inhibitors and their underlying mechanisms is highly significance for the successful utilization of these inhibitors in the treatment of diverse kidney disorders.


Assuntos
Diabetes Mellitus Tipo 2 , Nefropatias Diabéticas , Inibidores do Transportador 2 de Sódio-Glicose , Humanos , Inibidores do Transportador 2 de Sódio-Glicose/uso terapêutico , Nefropatias Diabéticas/tratamento farmacológico , Nefropatias Diabéticas/etiologia , Diabetes Mellitus Tipo 2/tratamento farmacológico , Hipoglicemiantes/uso terapêutico , Hipoglicemiantes/farmacologia , Rim
3.
Int J Mol Sci ; 24(17)2023 Aug 31.
Artigo em Inglês | MEDLINE | ID: mdl-37686364

RESUMO

Inflammation is a crucial pathological feature in cancers and kidney diseases, playing a significant role in disease progression. Cyclin-dependent kinases CDK4 and CDK6 not only contribute to cell cycle progression but also participate in cell metabolism, immunogenicity and anti-tumor immune responses. Recently, CDK4/6 inhibitors have gained approval for investigational treatment of breast cancer and various other tumors. Kidney diseases and cancers commonly exhibit characteristic pathological features, such as the involvement of inflammatory cells and persistent chronic inflammation. Remarkably, CDK4/6 inhibitors have demonstrated impressive efficacy in treating non-cancerous conditions, including certain kidney diseases. Current studies have identified the renoprotective effect of CDK4/6 inhibitors, presenting a novel idea and potential direction for treating kidney diseases in the future. In this review, we briefly reviewed the cell cycle in mammals and the role of CDK4/6 in regulating it. We then provided an introduction to CDK4/6 inhibitors and their use in cancer treatment. Additionally, we emphasized the importance of these inhibitors in the treatment of kidney diseases. Collectively, growing evidence demonstrates that targeting CDK4 and CDK6 through CDK4/6 inhibitors might have therapeutic benefits in various cancers and kidney diseases and should be further explored in the future.


Assuntos
Antineoplásicos , Nefropatias , Neoplasias , Animais , Antineoplásicos/farmacologia , Antineoplásicos/uso terapêutico , Terapias em Estudo , Divisão Celular , Inflamação , Nefropatias/tratamento farmacológico , Mamíferos , Neoplasias/tratamento farmacológico
4.
Bioengineered ; 13(4): 10665-10678, 2022 04.
Artigo em Inglês | MEDLINE | ID: mdl-35470759

RESUMO

Abnormal proliferation and migration of vascular smooth muscle cell (VSMC) is a hallmark of vascular neointima hyperplasia. Perilipin 5 (Plin5), a regulator of lipid metabolism, is also confirmed to be involved in vascular disorders, such as microvascular endothelial dysfunction and atherosclerosis. To investigate the regulation and function of plin5 in the phenotypic alteration of VSMC, -an animal model of vascular intima hyperplasia was established in C57BL/6 J and Plin5 knockdown (Plin5±) mice by wire injure. Immunohistochemical staining was used to analyze neointima hyperplasia in artery. Ki-67, dihydroethidium immunofluorescence staining and wound healing assay were used to measure proliferation, reactive oxygen species (ROS) generation and migration of VSMC, respectively. Plin5 was downregulated in artery subjected to vascular injury and in VSMC subjected to platelet-derived growth factor (PDGF)-BB. Plin5 knockdown led to accelerated neointima hyperplasia, excessive proliferation and migration of VSMC after injury. In vitro, we observed increased ROS content in VSMC isolated from Plin5± mice. Antioxidative N-acetylcysteine (NAC) inhibited VSMC proliferation and migration induced by PDGF-BB or plin5 knockdown. More importantly, plin5-peroxlsome proliferator-activated receptor-γ coactivator (PGC)-1α interaction was also attenuated in VSMC after knockdown of plin5. Overexpression of PGC-1α suppressed PDGF-BB-induced ROS generation, proliferation, and migration in VSMC isolated from Plin5± mice. These data suggest that plin5 serves as a potent regulator of VSMC proliferation, migration, and neointima hyperplasia by interacting with PGC-1α and affecting ROS generation.


Assuntos
Neointima , Fatores de Transcrição/metabolismo , Lesões do Sistema Vascular , Animais , Becaplermina , Movimento Celular/genética , Proliferação de Células , Células Cultivadas , Hiperplasia/metabolismo , Hiperplasia/patologia , Camundongos , Camundongos Endogâmicos C57BL , Músculo Liso Vascular/patologia , Neointima/genética , Neointima/metabolismo , Neointima/patologia , Perilipina-5/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Lesões do Sistema Vascular/genética , Lesões do Sistema Vascular/metabolismo , Lesões do Sistema Vascular/patologia
5.
Cancer Biomark ; 18(1): 1-9, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28035913

RESUMO

The mechanisms underlying oxaliplatin (OXA) resistance in colon cancer cells are not fully understood. MicroRNAs (miRNAs) play important roles in tumorigenesis and drug resistance. However, the relationship between miRNA and OXA resistance in colon cancer cells has not been previously explored. In this study, we utilized microRNA microarray analysis and real-time PCR to verify that miR-93, miR-191, miR-137, miR-181 and miR-491-3p were significantly down-regulated and that miR-96, miR-21, miR-22, miR-15b and miR-92 were up-regulated in both HCT-15/OXA and SW480/OXA cell lines. Blocking miR-137 caused a significant inhibition of OXA-induced cytotoxicity, therefore, miR-137 was chosen for further research. An in vitro cell viability assay showed that knockdown of miR-137 in HCT-15 and SW480 cells caused a marked inhibition of OXA-induced cytotoxicity. Moreover, we found that miR-137 was involved in repression of YBX1 expression through targeting its 3'-untranslated region. Furthermore, down-regulation of miR-137 conferred OXA resistance in parental cells, while over-expression of miR-137 sensitized resistant cells to OXA, which was partly rescued by YBX1 siRNA. The results of this study may aid the development of therapeutic strategies to overcome colon cancer cell resistance to OXA.


Assuntos
Neoplasias do Colo/tratamento farmacológico , Neoplasias do Colo/genética , MicroRNAs/genética , Compostos Organoplatínicos/farmacologia , Proteína 1 de Ligação a Y-Box/genética , Regiões 3' não Traduzidas , Antineoplásicos/farmacologia , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Proliferação de Células/genética , Neoplasias do Colo/metabolismo , Resistencia a Medicamentos Antineoplásicos , Técnicas de Silenciamento de Genes , Humanos , MicroRNAs/biossíntese , MicroRNAs/metabolismo , Oxaliplatina , Proteína 1 de Ligação a Y-Box/biossíntese , Proteína 1 de Ligação a Y-Box/metabolismo
6.
Journal of Forensic Medicine ; (6): 482-485, 2017.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-663688

RESUMO

Objective To analyse the cases of sudden death due to hyperthyroid heart disease,and explore the general information of deaths and the forensic pathological characteristics to provide reference evidence for forensic identification of such cases.Methods Six cases of sudden death due to hyperthyroid heart disease between 2001 and 2016 were selected from School of Forensic Medicine,China Medical University.The general information (gender and age),clinical manifestations,medical history,anatomical and histopathological findings,biochemical parameters and cause of death were analysed retrospectively.Results Most of the 6 patients had definite history of hyperthyroidism,and they all showed certain degrees of symptoms of cardiovascular disease;had obvious incentive factors of death;histopathological examination of thyroid conformed to the performances of diffuse toxic goiter;with increase of cardiac weight,dilatation of cardiac chambers,myocardial hypertrophy and focal necrosis;postmortem biochemical analyses of pericardial fluid could be used as an additional method for diagnostic of sudden death due to hyperthyroid heart disease.Conclusion The identification of death due to hyperthyroid heart disease should be based on the clinical history and the results of autopsy,histopathological examination,postmortem toxicology tests.The postmortem biochemical detection of thyroid and cardiac function should be performed if necessary.

7.
Guang Pu Xue Yu Guang Pu Fen Xi ; 34(8): 2298-302, 2014 Aug.
Artigo em Chinês | MEDLINE | ID: mdl-25474981

RESUMO

The concentration of inhalable particle is an important indicator in atmospheric environment monitor. Based on Mie scattering extinction, a precise testing instrument which can measure the concentration of inhalable particles at the atmospheric was designed by three-wavelength method in combination with the algorithm of distributed function. The dependence of extinction index on the spectrum was calculated based on Mie scattering theory in this article. Furthermore, the signal of time domain is integrated in the data processing to reduce the effect of error caused by multi-peak of spectra. The PM2.5 and PM10 were collected simultaneously in particle selection. Three different wave-lengths of lasers were coupled into an optical fiber by coupler (3 in 1) and passed through the sample cell. The attenuated light was detected by a PIN. Output of the detector was converted, amplified, displayed and stored by electronic system. Finally, the data were transmitted and shared in network through the 3G wireless module. The average particle size and concentration of inhalable particles were measured by this device at the same time. The technical specifications of the detector were verified by experiment, the experimental results indicate that the detection sensitivity of the system is 0.01 microg m(-3), the responsive time of system is approximately 90 s and it is suitable for measuring particulate matter concentrations of atmosphere.

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