Melatonin Ameliorates MI-Induced Cardiac Remodeling and Apoptosis through a JNKp53-Dependent Mechanism in Diabetes Mellitus
Joint Authors
Yang, Jian
Lu, Linhe
Ma, Jipeng
Sun, Mingming
Wang, Xiaowu
Gao, Erhe
Lu, Lintao
Yang, Lifang
Ren, Jun
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-14, 14 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-01-09
Country of Publication
Egypt
No. of Pages
14
Main Subjects
Abstract EN
Diabetes mellitus, a worldwide health threat, is considered an independent risk factor for cardiovascular diseases.
The overall cardiovascular risk of diabetes is similar to the one having one myocardial infarction (MI) attack although the precise impact of diabetes on MI-induced myocardial anomalies remains elusive.
Given that mortality following MI is much greater in diabetic patients compared to nondiabetic patients, this study was designed to examine the effect of melatonin on MI injury-induced myocardial dysfunction in diabetes.
Adult mice were made diabetic using high-fat feeding and streptozotocin (100 mg/kg body weight) prior to MI and were treated with melatonin (50 mg/kg/d, p.o.) for 4 weeks prior to assessment of cardiac geometry and function.
The MI procedure in diabetes displayed overt changes in cardiac geometry (chamber dilation and interstitial fibrosis) and functional anomalies (reduced fractional shortening and cardiomyocyte contractile capacity) in association with elevated c-Jun N-terminal kinase (JNK) phosphorylation and p53 level.
Melatonin treatment markedly attenuated cardiac dysfunction and myocardial fibrosis in post-MI diabetic mice.
Furthermore, melatonin decreased JNK phosphorylation, reduced p53 levels, and suppressed apoptosis in hearts from the post-MI diabetic group.
In vitro findings revealed that melatonin effectively counteracted high-glucose/high fat-hypoxia-induced cardiomyocyte apoptosis and contractile dysfunction through a JNK-mediated mechanism, the effects of which were impaired by the JNK activator anisomycin.
In summary, our study suggests that melatonin protects against myocardial injury in post-MI mice with diabetes, which offers a new therapeutic strategy for the management of MI-induced cardiac injury in diabetes.
American Psychological Association (APA)
Lu, Linhe& Ma, Jipeng& Sun, Mingming& Wang, Xiaowu& Gao, Erhe& Lu, Lintao…[et al.]. 2020. Melatonin Ameliorates MI-Induced Cardiac Remodeling and Apoptosis through a JNKp53-Dependent Mechanism in Diabetes Mellitus. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-14.
https://search.emarefa.net/detail/BIM-1203750
Modern Language Association (MLA)
Lu, Linhe…[et al.]. Melatonin Ameliorates MI-Induced Cardiac Remodeling and Apoptosis through a JNKp53-Dependent Mechanism in Diabetes Mellitus. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-14.
https://search.emarefa.net/detail/BIM-1203750
American Medical Association (AMA)
Lu, Linhe& Ma, Jipeng& Sun, Mingming& Wang, Xiaowu& Gao, Erhe& Lu, Lintao…[et al.]. Melatonin Ameliorates MI-Induced Cardiac Remodeling and Apoptosis through a JNKp53-Dependent Mechanism in Diabetes Mellitus. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-14.
https://search.emarefa.net/detail/BIM-1203750
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1203750