Diabetic cardiomyopathy: where we are and where we are going

Lee, Wang Soo; Kim, Jaetaek

doi:10.3904/kjim.2016.208

Cited by 129 publications

(196 citation statements)

References 140 publications

(216 reference statements)

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“…Myocardial use of glucose in case of chronic disease may be improved due to intake of the medicines, that can improve fatty acids metabolism and inhibit their oxidation [215,216].…”

Section: Correction Of Vascular Endothelial Dysfunctionmentioning

confidence: 99%

“…However, the following factors do not allow to implement its use: the degree of inhibition of fatty acids metabolism is limited by physiological indicators; ranolazine prescription associates with the possibility of QTc interval prolongation [216,218].…”

Section: Ranolazinementioning

confidence: 99%

“…Nebivolol, a β 1 -antagonist with β 2,3 -agonist property, improves endothelium-dependent vasodilator responses in patients with essential hypertension [212][213][214][215][216][217][218][219][220][221][222][223][224]. The effect of nebivolol on endothelial function appears to be mediated by increasing NO release and reducing prothrombotic blood levels of fibrinogen, homocysteine and plasminogen activator inhibitor-1 [223,224].…”

Section: Beta Blockersmentioning

confidence: 99%

“…Anti-ischemic properties of trimetazidine do not depend on changes in hemodynamics and are associated with a distinct recovery of mechanical function after ischemia, which makes it recognized as cardyo-cytoprotective agent. Trimetazidine prescription improves glucose metabolism; reduces endothelin-1 among patients with diabetic cardiomyopathy, that is taken to have effect on the vascular endothelium; accompanied by a significant positive changes in ejection fraction (EF) parameters among patients with HF; improves quality of life parameters and NYHA functional class [215,216]. 9.11.2.…”

mentioning

confidence: 99%

“…Perhexiline prescription to patients with heart failure significantly contributes to the improvement of EF, VO 2 max and quality of life. Unfortunately, the clinical use of this medicament is limited because of the risk of hepatotoxicity and PNP [216,217].…”

mentioning

confidence: 99%

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Diabetic Cardiovascular Neuropathy

Serhiyenko¹,

Publisher²,

Serhiyenko³

2018

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Cardiac autonomic neuropathy (CAN) is a serious complication of diabetes mellitus, that is strongly associated with increased risk of cardiovascular mortality. Although it is common complication, the significance of CAN has not been fully appreciated and there are no unified treatment algorithms for today. In this review we have analyzed the existing data about the known risk factors, screening and diagnostic algorithm, staging of CAN and possible treatment, including effectiveness of lifestyle modification, intensive glycemic control; treatment of diabetic dyslipidemia; antioxidants; vitamins; correction of vascular endothelial dysfunction; prevention and treatment of thrombosis; treatment of orthostatic hypotension. Conclusion 88References 89 Abbreviations list 108Victoria Serhiyenko, Alexandr Serhiyenko 7 ABOUT THE AUTHORSVictoria A Serhiyenko, MD, PhD in Medicine Sciences, DMSc, Associate Professor of the Department of Endocrinology, Lviv National Medical University named by Danylo Halitsky, Lviv, Ukraine. At the moment she is working on the problems concerted with the revelation of the correlating connections between activities of some metabolic, hormonal and other parameter, and state of the proand anti-inflammatory factors in blood in patients with diabetes mellitus which depends on the character of diabetic complications. The second part of his scientific work is the research of the effectively of the benfotiamine in treatment and prevention of diabetic complications in clinical practice.Victoria Serhiyenko has published 238 scientific papers. These works are devoted to the problems of pathogenesis, diagnosis and treatment, prevention of the diabetic cardiovascular autonomic neuropathy.Alexandr A Serhiyenko, MD, PhD in Medicine Sciences, DMSc, Professor of the Department of Endocrinology, Lviv National Medical University named by Danylo Halitsky, Lviv, Ukraine. At the moment he is working on the problems concerted with the revelation of the correlating connections between activities of some metabolic parameters in patients with diabetes mellitus which depends on the character of diabetic complications. The second part of her scientific work is the research of the effectively of the benfotiamine in treatment and prevention of diabetic complications in clinical practice.Alexandr Serhiyenko has published 613 scientific papers. These works are devoted to the problems of pathogenesis, diagnosis and treatment, prevention of the diabetic complications.

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“…Myocardial use of glucose in case of chronic disease may be improved due to intake of the medicines, that can improve fatty acids metabolism and inhibit their oxidation [215,216].…”

Section: Correction Of Vascular Endothelial Dysfunctionmentioning

confidence: 99%

Section: Ranolazinementioning

confidence: 99%

Section: Beta Blockersmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Diabetic Cardiovascular Neuropathy

Serhiyenko¹,

Publisher²,

Serhiyenko³

2018

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miR‐34a attenuates myocardial fibrosis in diabetic cardiomyopathy mice via targeting Pin‐1

Zhang

Bai

2020

Cell Biology International

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Diabetic cardiomyopathy (DCM) is characterized by myocardial hypertrophy and fibrosis. This study aimed to investigate the effects of microRNA (miR)‐34a on myocardial fibrosis in DCM and its potential mechanism of targeting Pin‐1 signaling. Vimentin and Pin‐1 proteins in mouse cardiac tissues were detected by immunohistochemical staining. Locked nucleic acid in situ hybridization was used to measure miR‐34a expression in cardiac tissues. Primary mouse cardiac fibroblasts (CFs) were transfected with a mimics control/miR‐34a mimics or Pin‐1 plasmid and cultured in high‐glucose (HG) Dulbecco's modified Eagle's medium. The miR‐34a levels were measured by quantitative polymerase chain reaction. The apoptosis and viability of transfected cells were detected by the terminal deoxynucleotidyl transferase dUTP nick end labeling and Cell Counting Kit‐8 assays respectively. A cell migration experiment and dual‐luciferase reporter assay were also performed. The body weight and fasting blood glucose of DCM mice were significantly higher than those in the control (CTL) group. In addition, DCM mice had decreased serum insulin levels and impaired cardiac function. The number of CFs in the DCM group was higher than in the CTL group and Pin‐1 expression was upregulated. The expression level of miR‐34a in the cardiac tissue of mice in the DCM group was obviously downregulated compared with the CTL group. The HG stimulation of CFs for 48 h significantly downregulated the expression level of miR‐34a and was associated with increased Type I collagen expression, cell viability, and migration and decreased apoptosis. However, these effects could be reversed by overexpressing miR‐34a in HG‐induced CFs. Furthermore, we found that Pin‐1 was a direct target of miR‐34a. Our results suggest that miR‐34a can attenuate myocardial fibrosis in DCM by reducing Type I collagen production, cell viability, and migration and increasing the apoptosis of CFs by targeting Pin‐1 signaling.

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Targeting TRAF3IP2 alleviates high glucose‐induced cardiomyocyte inflammation and apoptosis

Wei

Yan

2021

Drug Development Research

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To clarify the role of TRAF3IP2 in high glucose (HG)‐stimulated cardiomyocyte inflammation and apoptosis and its action mechanism. SiRNA plasmid of TRAF3IP2 was constructed and transfected into HG‐stimulated cardiomyocytes to silence TRAF3IP2. The expression of TRAF3IP2 was determined by quantitative polymerase chain reaction (qPCR) and western blot. Cell viability and cytotoxicity were first observed using cell counting kit‐8 and lactate dehydrogenase assays. The inflammatory injury of the cardiomyocytes was then examined by real time‐qPCR (RT‐qPCR) and western blot. The oxidative stress of the cardiomyocytes was evaluated using reactive oxygen species assay kit, RT‐qPCR, western blot and enzyme activity assay kit. Next, cell apoptosis was detected employing TUNEL and western blot. Finally, RT‐qPCR and western blot were performed to investigate the effects of inhibitors of dipeptidyl peptidase‐4, including saxagliptin, empagliflozin and linagliptin, on TRAF3IP2. TRAF3IP2 expression was found to be increased in HG‐stimulated cardiomyocytes. TRAF3IP2 interference inhibited HG‐induced cell viability loss, cytotoxicity, inflammatory response, oxidative stress and apoptosis of the cardiomyocytes. Moreover, saxagliptin, empagliflozin and linagliptin inhibited the expression of TRAF3IP2. TRAF3IP2 interference alleviates HG‐induced inflammation and apoptosis of cardiomyocytes. The result suggests that TRAF3IP2 may be a promising therapeutic target in treating diabetic cardiomyopathy.

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Diabetic cardiomyopathy: where we are and where we are going

Cited by 129 publications

References 140 publications

Diabetic Cardiovascular Neuropathy

Diabetic Cardiovascular Neuropathy

miR‐34a attenuates myocardial fibrosis in diabetic cardiomyopathy mice via targeting Pin‐1

Targeting TRAF3IP2 alleviates high glucose‐induced cardiomyocyte inflammation and apoptosis

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