Factors Associated with the e-Health Literacy Among Older Adults with Chronic Obstructive Pulmonary Disease: A Cross-Sectional Study.

Background: The telemanagement model in chronic diseases needs older patients to have a certain level of e-Health literacy. According to Electronic Health Literacy model, factors associated with the e-Health literacy among older patients could be comprehensively investigated from individual, situational, and environmental aspects. Objectives: To investigate the e-Health literacy levels among older patients with chronic obstructive pulmonary disease (COPD) and explore associated factors. Methods: A cross-sectional study was conducted among older patients with COPD. The e-Health Literacy Scale was used to measure individuals' e-Health literacy. The multiple linear regression was applied to identify factors associated with e-Health literacy. Results: A total of 230 responses were included in the final analysis. The average score of e-Health literacy for older COPD patients was 24.66 (6.86). After adjusting the model, the results of multiple linear regression demonstrated that aging attitudes (B = 0.067, p < 0.001), technophobia (B = -0.285, p < 0.001), and self-efficacy (B = 0.431, p < 0.001) accounted for 68.3% (p < 0.001) of the total variation in e-Health literacy. Conclusion: This study identifies significant correlations of technophobia, aging attitudes, and self-efficacy, respectively, with e-Health literacy, and self-efficacy and technophobia may be constant predictive factors of e-Health literacy. In the future, intervention research on e-Health literacy should be conducted from a social psychology perspective, with particular emphasis on addressing negative aging attitudes and technophobia. That will promote the tele-management model of chronic diseases. Trial Registration: Chinese Clinical Trial Registry (ChiCTR): ChiCTR1900028563; http://apps.who.int/trialsearch/default.aspx.

Mechanistic insights into heat shock protein 27, a potential therapeutic target for cardiovascular diseases.

Heat shock protein 27 (HSP27) is a small chaperone protein that is overexpressed in a variety of cellular stress states. It is involved in regulating proteostasis and protecting cells from multiple sources of stress injury by stabilizing protein conformation and promoting the refolding of misfolded proteins. Previous studies have confirmed that HSP27 is involved in the development of cardiovascular diseases and plays an important regulatory role in this process. Herein, we comprehensively and systematically summarize the involvement of HSP27 and its phosphorylated form in pathophysiological processes, including oxidative stress, inflammatory responses, and apoptosis, and further explore the potential mechanisms and possible roles of HSP27 in the diagnosis and treatment of cardiovascular diseases. Targeting HSP27 is a promising future strategy for the treatment of cardiovascular diseases.

The role of exercise-induced myokines in promoting angiogenesis.

Ischemic diseases are a major cause of mortality or disability in the clinic. Surgical or medical treatment often has poor effect on patients with tissue and organ ischemia caused by diffuse stenoses. Promoting angiogenesis is undoubtedly an effective method to improve perfusion in ischemic tissues and organs. Although many animal or clinical studies tried to use stem cell transplantation, gene therapy, or cytokines to promote angiogenesis, these methods could not be widely applied in the clinic due to their inconsistent experimental results. However, exercise rehabilitation has been written into many authoritative guidelines in the treatment of ischemic diseases. The function of exercise in promoting angiogenesis relies on the regulation of blood glucose and lipids, as well as cytokines that secreted by skeletal muscle, which are termed as myokines, during exercise. Myokines, such as interleukin-6 (IL-6), chemokine ligand (CXCL) family proteins, irisin, follistatin-like protein 1 (FSTL1), and insulin-like growth factor-1 (IGF-1), have been found to be closely related to the expression and function of angiogenesis-related factors and angiogenesis in both animal and clinical experiments, suggesting that myokines may become a new molecular target to promote angiogenesis and treat ischemic diseases. The aim of this review is to show current research progress regarding the mechanism how exercise and exercise-induced myokines promote angiogenesis. In addition, the limitation and prospect of researches on the roles of exercise-induced myokines in angiogenesis are also discussed. We hope this review could provide theoretical basis for the future mechanism studies and the development of new strategies for treating ischemic diseases.

Intestinal Flora: A Potential New Regulator of Cardiovascular Disease.

Although substantial progress has been made in reducing the burden of the disease by preventing the risk factors of cardiovascular disease (CVD), potential risk factors still exist and lead to its progression. In recent years, numerous studies have revealed that intestinal flora can interfere with the physiological processes of the host through changes in composition and function or related metabolites. Intestinal flora thus affects the occurrence and development of a variety of CVDs, including atherosclerosis, ischemic heart disease, and heart failure. Moreover, studies have found that interventions for intestinal flora and its metabolites provide new opportunities for CVD treatment. This article mainly discusses the interaction between the human intestinal flora and its metabolites, the occurrence and development of CVD, and the potential of intestinal flora as a new target for the diagnosis and treatment of CVD.

Role of GTPase-Dependent Mitochondrial Dynamins in Heart Diseases.

Heart function maintenance requires a large amount of energy, which is supplied by the mitochondria. In addition to providing energy to cardiomyocytes, mitochondria also play an important role in maintaining cell function and homeostasis. Although adult cardiomyocyte mitochondria appear as independent, low-static organelles, morphological changes have been observed in cardiomyocyte mitochondria under stress or pathological conditions. Indeed, cardiac mitochondrial fission and fusion are involved in the occurrence and development of heart diseases. As mitochondrial fission and fusion are primarily regulated by mitochondrial dynamins in a GTPase-dependent manner, GTPase-dependent mitochondrial fusion (MFN1, MFN2, and OPA1) and fission (DRP1) proteins, which are abundant in the adult heart, can also be regulated in heart diseases. In fact, these dynamic proteins have been shown to play important roles in specific diseases, including ischemia-reperfusion injury, heart failure, and metabolic cardiomyopathy. This article reviews the role of GTPase-dependent mitochondrial fusion and fission protein-mediated mitochondrial dynamics in the occurrence and development of heart diseases.

Crosstalk between extracellular vesicles and autophagy in cardiovascular pathophysiology.

Extracellular vesicles are composed of loaded soluble substances and lipid bilayers; these include apoptotic bodies, exosomes, and microvesicles. Extracellular vesicles, as carriers of biological information between cells, have been recognized for their role in the diagnosis and treatment of cardiovascular diseases. The biogenesis of extracellular vesicles is closely related to autophagy. Moreover, extracellular vesicles further affect autophagy levels in target cells through their transmitted contents. Autophagy is a catabolic cell process that maintains cell homeostasis by eliminating misfolded proteins and damaged organelles. Existing studies have revealed that extracellular vesicles and autophagy share molecular mechanisms with notable crosstalk, including, perspectives such as amphisomes and "secretory autophagy." In this review, we first introduce the biogenesis of extracellular vesicles and the classic views of autophagy before moving onto the crosstalk between extracellular vesicles and autophagy. Finally, we discuss the research progress of extracellular vesicles and autophagy in cardiovascular pathophysiology.

MicroRNA-103 Protects Coronary Artery Endothelial Cells against H2O2-Induced Oxidative Stress via BNIP3-Mediated End-Stage Autophagy and Antipyroptosis Pathways.

Endothelial cell damage caused by oxidative stress is widely considered to be a triggering event in atherosclerosis (AS). However, the specific effect elicited by autophagy in endothelial cells undergoing oxidative stress remains controversial, especially during end-stage autophagy. The inhibition of end-stage autophagy has been reported to increase cell pyroptosis and contribute to endothelial damage. Several studies have shown that microRNA-103 is involved in end-stage autophagy; however, its specific mechanism of action is not yet characterized. In this study, we addressed the regulatory role of miR-103 in autophagy during oxidative stress of endothelial cells. Hydrogen peroxide (H2O2) treatment was used as an in vitro model of oxidative stress. MTS and ROS levels were measured to evaluate cell activity. qRT-PCR was used to detect the expression of miR-103. Autophagy was examined using western blot, immunofluorescence staining, and electron microscopy, while western blot analysis detected pyroptosis-related proteins. Results show that miR-103 expression decreased under oxidative stress. Further, miR-103 repressed transcription of Bcl-2/adenovirus E1B 19 kDa interacting protein (BNIP3). The oxidative stress caused by H2O2 caused cell damage from 2 hours (P < 0.05) and increased the level of intracellular reactive oxygen species (P < 0.05); at the same time, the damage could be further aggravated by the stimulation of bafA1 (P < 0.05). Under the stimulation of H2O2, the expression of miR-103 decreased (P < 0.05). However, high expression of miR-103 could reduce the accumulation of LC3II and P62 (P < 0.05) by inhibiting the downstream target gene Bcl-2/adenovirus E1B 19 kDa interacting protein (BNIP3), thus reducing the occurrence of cell pyroptosis (P < 0.05). This process could be blocked by end-stage autophagy inhibitor bafA1 (P < 0.05), which further indicated that miR-103 affected cell injury by autophagy. On the contrary, the low expression of miR-103 promoted the accumulation of autophagy protein and increased the occurrence of pyroptosis (P < 0.05). In conclusion, inhibition of miR-103 restrained end-stage of autophagy by regulating BNIP3, thus changing the occurrence of cell pyroptosis.

Awareness of hypertension and related factors in northeastern China: a cross-sectional study.

Timely awareness of hypertension is among the most crucial components in reducing the burden of hypertension. However, there is limited information about the awareness of hypertension in northern China. Therefore, in this cross-sectional study, we aimed to investigate the awareness of hypertension and its associated factors in the Jilin province in China; the study was conducted between July 2014 and December 2015 in four cities and four rural counties in the Jilin province as part of a national study. A stratified multistage random-sampling method was used to select a representative sample: a total of 15,206 participants aged ≥15 years were initially recruited, among which 14,956 were finally included in the survey. The awareness of hypertension in the Jilin province was found to be 42.3%. Moreover, the awareness of hypertension was associated with age, sex, region, marital status, body mass index, and family history of hypertension or coronary artery disease. Employment was associated with a lower awareness in rural areas, whereas high education was associated with a higher awareness in urban areas. Policies targeting specific subgroups may be helpful in increasing the awareness of hypertension in the Jilin province.

The role of lncRNA MALAT1 in cardiovascular disease.

Cardiovascular disease (CVD) is the first leading cause of death worldwide. Understanding the molecular mechanism of signaling pathways involved in pathology of CVD is benefit for targeted therapeutics. Recently, long non-coding RNAs (lncRNAs) are found and involved in regulation of pathology of CVD at different levels. Among them, MALAT1 attracted more attention as it was profoundly expressed in endothelial cells or cardiomyocytes in response to the risk factors of CVD, such as hypoxia, high glucose, cytokine, and oxidative stress. In this review, we summarize recent progresses in research on the molecular mechanism of MALAT1 on regulating the pathophysiological processes of CVD as well as its potential therapeutic applications.

Effect of Hypoxia-Induced MicroRNA-210 Expression on Cardiovascular Disease and the Underlying Mechanism.

Cardiovascular diseases have high morbidity and mortality rates worldwide, and their treatment and prevention are challenging. MicroRNAs are a series of noncoding RNAs with highly conserved sequences and regulate gene expression by inhibiting mRNA transcription or degrading targeting proteins. MicroRNA-210 is significantly upregulated during hypoxia and plays a protective role by inhibiting apoptosis and regulating cell proliferation, differentiation, migration, mitochondrial metabolism, and angiogenesis in hypoxic cells. MicroRNA-210 expression is altered in cardiovascular diseases such as atherosclerosis, acute myocardial infarction, preeclampsia, aortic stenosis, and heart failure, and overexpression of microRNA-210 in some of these diseases exerts protective effects on target organs. Furthermore, chronically upregulated miR-210 potentially plays a marked pathogenic role in specific situations. This review primarily focuses on the upstream pathways, downstream targets, clinical progress in cardiovascular disease, and potential applications of microRNA-210.

Long non-coding RNAs in coronary atherosclerosis.

Coronary atherosclerosis (CAS), a leading cause of cardiovascular disease, is a major cause of death worldwide. CAS is a chronic disease in the aorta that can be caused by dyslipidemia, abnormal glucose metabolism, endothelial cell dysfunction, vascular smooth muscle cell (VSMC) or fibrous connective tissue hyperplasia, immune inflammatory reactions, and many other factors. The pathogenesis of CAS is not fully understood, as it is a complex lesion complicated by multiple factors. Damage-response theories have put forward endothelial cell (EC) injury as the initiating factor for CAS; the addition of lipid metabolism disorders may enhance monocyte adhesion, increase the proliferation and migration of fibroblasts and VSMCs, and accelerate the development of CAS. Furthermore, inflammatory and immune responses can create a vicious cycle of endothelial injury, which also plays key roles in the formation of CAS. Therefore, in order to elucidate the mechanisms controlling CAS, it is important to study the etiology of vascular cell dysfunction, abnormal energy and metabolism disorders, and immune and inflammatory reactions. Non-coding RNAs play regulatory roles in the pathogenesis of CAS, especially long non-coding RNAs (lncRNAs); lncRNAs have recently become a major focus for cardiovascular disease mechanisms, as they play numerous roles in the progression of CAS. Therefore, in this review, we discuss the role of lncRNAs in the pathogenesis of coronary CAS, and their role in the prevention and treatment of coronary CAS.

Prevalence and distribution of hypertension and related risk factors in Jilin Province, China 2015: a cross-sectional study.

OBJECTIVE: This study aimed to investigate the prevalence and distribution of hypertension and its related factors in Jilin province, China. DESIGN: A cross-sectional study in four cities and four rural counties in Jilin as part of a national Chinese study. PARTICIPANTS AND SETTING: A total of 15 206 participants who were ≥15 years old and were selected using a stratified multistage random sampling method. MAIN OUTCOME MEASURES: The prevalence of hypertension. RESULTS: The prevalence of hypertension in Jilin province was 24.7%. Moreover, the prevalence of hypertension increased with age in both sexes, and was higher in men than in women. The modifiable factors that were associated with hypertension were body mass index, smoking and alcohol drinking. The risk factors identified are similar to those in southern China, except smoking, which has no association with hypertension prevalence in the South. CONCLUSIONS: Age, sex, body mass index, smoking and alcohol drinking were risk factors of hypertension. Control of these related risk factors, especially smoking, may be helpful in the treatment and management of hypertension in Jilin province.

MicroRNA-210 Modulates the Cellular Energy Metabolism Shift During H2O2-Induced Oxidative Stress by Repressing ISCU in H9c2 Cardiomyocytes.

BACKGROUND/AIMS: The myocardial energy metabolism shift is one of the most important pathological features of ischemic heart disease (IHD). Although several microRNAs (miRs) are involved in the regulation of myocardial energy metabolism, their exact effects and underlying mechanisms remain unclear. The aim of this study was to investigate whether microRNA(miR-210) regulates the energy metabolism shift during oxidative stress in H9c2 cardiomyocytes. METHODS: Cell survival was analyzed via CCK assay. The energy metabolism shift was detected by lactate assay, ATP assay and RT2 profiler glucose metabolism PCR array. Protein and mRNA expression levels were determined by western blot and qPCR. We also used kits to detect the activity of Complex I, Sirt3 and the NAD+/NADH ratio. RESULTS: We determined that miR-210 promoted the energy metabolism shift. The iron-sulfur cluster assembly protein (ISCU) was a target of miR-210. Additionally, we detected the activity of complex I and found that miR-210 inhibits mitochondrial respiration. Interestingly, miR-210 may also indirectly regulate SIRT3 by regulating ISCU. CONCLUSION: Our results confirm that miR-210 is essential and sufficient for modulating the cellular energy metabolism shift during H2O2-induced oxidative stress in H9c2 cardiomyocytes by targeting ISCU.

PEGylated stereocomplex polylactide coating of stent for upregulated biocompatibility and drug storage.

Treatment of coronary heart disease by percutaneous coronary intervention (PCT) is usually limited to the high restenosis rate after implantation of bare-metal stent. To solve the problem, the coating of PEGylated stereocomplex poly(l-lactide) (PEG-cPLA) was utilized on the surface modification of stainless steel (SS) sheet. Specifically, the 3-aminopropyltriethoxysilane (APTES)-modified methoxy-poly(ethylene glycol)-poly(d-lactide) (mPEG-PDLA) was grafted onto the surface of hydroxylated SS sheet through coupling reaction, and poly(l-lactide)-poly(ethylene glycol)-poly(l-lactide) (PLLA-PEG-PLLA) was coated onto the surface through stereocomplex interaction between DLA and LLA units. The increase of contact angle firstly confirmed the changes of surface composition and hydrophilicity for the PEG-scPLA-modified SS sheet. The decreased fibrinogen adsorption, down-regulated platelet activation, and improved adhesion of human umbilical vein endothelial cells (HUVECs) indicated the excellent biocompatibility of PEG-scPLA-modified SS sheet. In addition, the drug loading capability of SS sheet was greatly upregulated through the formation of scPLA coating on the surface, where fluorescein (FLU) was chosen as a model molecule. Overall, the surface modification of SS sheet with PEG-scPLA could enhance the comprehensive performances, such as biocompatibility and drug loading capability, demonstrating that PEG-scPLA is a promising coating of coronary stent for PCT.

MicroRNA-210 alleviates oxidative stress-associated cardiomyocyte apoptosis by regulating BNIP3.

Oxidative stress-induced myocardial apoptosis and necrosis are involved in ischemia/reperfusion (I/R) injury. This study was performed to investigate microRNA (miR)-210's role in oxidative stress-related myocardial damage. The expression of miR-210 was upregulated in myocardial tissues of I/R rats, while that of Bcl-2 adenovirus E1B 19kDa-interacting protein 3 (BNIP3) was downregulated. To simulate in vivo oxidative stress, H9c2 cells were treated with H2O2 for 48 h. MiR-210 level was increased upon H2O2 stimulation, peaked at 8 h, and then decreased. An opposite expression pattern of BNIP3 was observed. BNIP3 was demonstrated as a direct target of miR-210 via luciferase reporter assay. H2O2-induced cell apoptosis was attenuated by miR-210 mimics, whereas aggravated by miR-210 inhibitor. MiR-210 knockdown-induced cell apoptosis in presence of H2O2 was attenuated by BNIP3 siRNA. Our work demonstrates that miR-210 plays a protective role in H2O2-induced cardiomyocyte apoptosis at least by regulating the pro-apoptotic BNIP3.

Protection of Human Umbilical Vein Endothelial Cells against Oxidative Stress by MicroRNA-210.

Oxidative stress induces endothelial cell apoptosis and promotes atherosclerosis development. MicroRNA-210 (miR-210) is linked with apoptosis in different cell types. This study aimed to investigate the role of miR-210 in human umbilical vein endothelial cells (HUVECs) under oxidative stress and to determine the underlying mechanism. HUVECs were treated with different concentrations of hydrogen peroxide (H2O2), and cell viability was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and ATP assay. To evaluate the role of miR-210 in H2O2-mediated apoptosis, gain-and-loss-of-function approaches were used, and the effects on apoptosis and reactive oxygen species (ROS) level were assayed using flow cytometry. Moreover, miR-210 expression was detected by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), and expression of the following apoptosis-related genes was assessed by qRT-PCR and Western blot at the RNA and protein level, respectively: caspase-8-associated protein 2 (CASP8AP2), caspase-8, and caspase-3. The results showed that H2O2 induced apoptosis in HUVECs in a dose-dependent manner and increased miR-210 expression. Overexpression of miR-210 inhibited apoptosis and reduced ROS level in HUVECs treated with H2O2. Furthermore, miR-210 downregulated CASP8AP2 and related downstream caspases at protein level. Thus, under oxidative stress, miR-210 has a prosurvival and antiapoptotic effect on HUVECs by reducing ROS generation and downregulating the CASP8AP2 pathway.

MiR-186 Inhibited Migration of NSCLC via Targeting cdc42 and Effecting EMT Process.

In this study, qRT-PCR was employed to identify that miR-186 expression level in NSCLC tissues are highly associated with lymph node metastasis. In addition, through the application of western blotting, luciferase assay and qRT-PCR, it was found that miR-186 targeted 3'UTR of cdc42 mRNA and down-regulated cdc42 protein level in a post-transcriptional manner. Transwell assay indicated that cdc42 partially reversed the effect of miR-186 mimics. Besides, miR-186 was proved to regulate EMT by influencing biomarkers of this process and cell adhesion ability. Thus, miR-186 is a potential target for NSCLC therapy. miR-186 is proposed to be one of tumor-suppressors and may serve as a therapeutic target in NSCLC treatment.

MicroRNA-135a Regulates Apoptosis Induced by Hydrogen Peroxide in Rat Cardiomyoblast Cells.

Oxidative stress and apoptosis are the most important pathologic features of ischemic heart disease. Recent research has indicated that microRNAs (miRs) play an essential role in apoptosis. However, whether miRs might regulate B cell lymphoma-2 (Bcl-2) protein in apoptosis during ischemic heart disease is still unclear. The aim of this study, therefore, was to confirm the regulation of microRNA-135a (miR-135a) in oxidative stress injuries induced by hydrogen peroxide (H2O2) in rat cardiomyoblast cells H9c2. To this end, we analyzed the effects of H2O2 treatment on miR-135a expression in rat cardiomyocytes. Furthermore, we upregulated and inhibited miR-135a using mimics and inhibitors, respectively, and examined the effects on cell viability and apoptosis-related proteins. We observed that miR-135a was markedly up-regulated under H2O2 treatment in rat cardiomyoblast cells. Overexpression of miR-135a blocked the Bcl-2 protein and enhanced the apoptosis induced by H2O2, and miR-135a inhibition restored Bcl-2 protein expression. Interestingly, miR-135a inhibition did not attenuate H2O2-induced apoptosis with Bcl-2 knockdown. The results of the present study indicate that miR-135a regulates H2O2-induced apoptosis in H9c2 cells via targeting Bcl-2, and that miR-135a may be a novel therapeutic target for ischemic heart disease.

HSP27 Inhibits Homocysteine-Induced Endothelial Apoptosis by Modulation of ROS Production and Mitochondrial Caspase-Dependent Apoptotic Pathway.

Objectives. Elevated plasma homocysteine (Hcy) could lead to endothelial dysfunction and is viewed as an independent risk factor for atherosclerosis. Heat shock protein 27 (HSP27), a small heat shock protein, is reported to exert protective effect against atherosclerosis. This study aims to investigate the protective effect of HSP27 against Hcy-induced endothelial cell apoptosis in human umbilical vein endothelial cells (HUVECs) and to determine the underlying mechanisms. Methods. Apoptosis, reactive oxygen species (ROS), and mitochondrial membrane potential (MMP) of normal or HSP27-overexpressing HUVECs in the presence of Hcy were analyzed by flow cytometry. The mRNA and protein expression levels were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Results. We found that Hcy could induce cell apoptosis with corresponding decrease of nitric oxide (NO) level, increase of endothelin-1 (ET-1), intracellular adhesion molecule-1 (ICAM-1), vascular cellular adhesion molecule-1 (VCAM-1), and monocyte chemoattractant protein-1 (MCP-1) levels, elevation of ROS, and dissipation of MMP. In addition, HSP27 could protect the cell against Hcy-induced apoptosis and inhibit the effect of Hcy on HUVECs. Furthermore, HSP27 could increase the ratio of Bcl-2/Bax and inhibit caspase-3 activity. Conclusions. Therefore, we concluded that HSP27 played a protective role against Hcy-induced endothelial apoptosis through modulation of ROS production and the mitochondrial caspase-dependent apoptotic pathway.