Gaseous signal molecule SO <sub>2</sub> regulates autophagy through PI3K/AKT pathway inhibits cardiomyocyte apoptosis and improves myocardial fibrosis in rats with type II diabetes

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Abstract

Myocardial fibrosis is a key link in the occurrence and development of diabetic cardiomyopathy. Its etiology is complex, and the effect of drugs is not good. Cardiomyocyte apoptosis is an important cause of myocardial fibrosis. The purpose of this study was to investigate the effect of gaseous signal molecule sulfur dioxide (SO ₂) on diabetic myocardial fibrosis and its internal regulatory mechanism. Masson and TUNEL staining, Western-blot, transmission electron microscopy, RT-qPCR, immunofluorescence staining, and flow cytometry were used in the study, and the interstitial collagen deposition, autophagy, apoptosis, and changes in phosphatidylinositol 3-kinase (PI3K)/AKT pathways were evaluated from in vivo and in vitro experiments. The results showed that diabetic myocardial fibrosis was accompanied by cardiomyocyte apoptosis and down-regulation of endogenous SO ₂-producing enzyme aspartate aminotransferase (AAT) _1/2. However, exogenous SO ₂ donors could up-regulate AAT _1/2, reduce apoptosis of cardiomyocytes induced by diabetic rats or high glucose, inhibit phosphorylation of PI3K/AKT protein, up-regulate autophagy, and reduce interstitial collagen deposition. In conclusion, the results of this study suggest that the gaseous signal molecule SO ₂ can inhibit the PI3K/AKT pathway to promote cytoprotective autophagy and inhibit cardiomyocyte apoptosis to improve myocardial fibrosis in diabetic rats. The results of this study are expected to provide new targets and intervention strategies for the prevention and treatment of diabetic cardiomyopathy.

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Diabetic Cardiomyopathy

James Sowers, Guanghong Jia, Michael A. Hill (2018)

Heart failure and related morbidity and mortality are increasing at an alarming rate, in large part, because of increases in aging, obesity, and diabetes mellitus. The clinical outcomes associated with heart failure are considerably worse for patients with diabetes mellitus than for those without diabetes mellitus. In people with diabetes mellitus, the presence of myocardial dysfunction in the absence of overt clinical coronary artery disease, valvular disease, and other conventional cardiovascular risk factors, such as hypertension and dyslipidemia, has led to the descriptive terminology, diabetic cardiomyopathy. The prevalence of diabetic cardiomyopathy is increasing in parallel with the increase in diabetes mellitus. Diabetic cardiomyopathy is initially characterized by myocardial fibrosis, dysfunctional remodeling, and associated diastolic dysfunction, later by systolic dysfunction, and eventually by clinical heart failure. Impaired cardiac insulin metabolic signaling, mitochondrial dysfunction, increases in oxidative stress, reduced nitric oxide bioavailability, elevations in advanced glycation end products and collagen-based cardiomyocyte and extracellular matrix stiffness, impaired mitochondrial and cardiomyocyte calcium handling, inflammation, renin-angiotensin-aldosterone system activation, cardiac autonomic neuropathy, endoplasmic reticulum stress, microvascular dysfunction, and a myriad of cardiac metabolic abnormalities have all been implicated in the development and progression of diabetic cardiomyopathy. Molecular mechanisms linked to the underlying pathophysiological changes include abnormalities in AMP-activated protein kinase, peroxisome proliferator-activated receptors, O-linked N-acetylglucosamine, protein kinase C, microRNA, and exosome pathways. The aim of this review is to provide a contemporary view of these instigators of diabetic cardiomyopathy, as well as mechanistically based strategies for the prevention and treatment of diabetic cardiomyopathy.

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Author and article information

Journal

Journal ID (nlm-ta): Korean J Physiol Pharmacol

Journal ID (iso-abbrev): Korean J Physiol Pharmacol

Title: The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology

Publisher: The Korean Physiological Society and The Korean Society of Pharmacology

ISSN (Print): 1226-4512

ISSN (Electronic): 2093-3827

Publication date (Print): 1 November 2022

Publication date (Electronic): 1 November 2022

Publication date PMC-release: 1 November 2022

Volume: 26

Issue: 6

Pages: 541-556

Affiliations

[1 ]Department of Pharmacy, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang 421000, China

[2 ]Department of Cardiology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang 421000, China

[3 ]Department of General Practice, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang 421000, China

[4 ]School of Pharmaceutical Science of University of South China, Hengyang 421000, China

[5 ]Department of Ultrasound Medicine, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang 421000, China

[6 ]Department of Critical Care Medicine, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, Hengyang 421000, China

[7 ]Department of Cardiology, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, Hengyang 421000, China

[8 ]Department of Cardiology, Shenzhen Longhua District Central Hospital, Longhua Central Hospital Affiliated Guang-dong Medical University, Shenzhen 518000, China

Author notes

[* ] Correspondence Chun Chu, E-mail: yjchuchun@ 123456163.com

Jun Yang, E-mail: yangjunketizu@ 123456163.com

Ting Xiao, E-mail: 1459593600@ 123456qq.com

[#]

These authors contributed equally to this work.

Author contributions: J.Z. and Q.W. were responsible for the execution of the experiments and the writing of the manuscript. T.Y., L.N., S.L., and J.Z. participated in molecular biology testing and experimental design, J.C. and Z.J. were responsible for the execution of experiments and data analysis. T.X., J.Y., and C.C. were responsible for the design of the experiment. All authors contributed to this work and approved the submitted version.

Article

Publisher ID: kjpp-26-6-541

DOI: 10.4196/kjpp.2022.26.6.541

PMC ID: 9614393

PubMed ID: 36302628

SO-VID: d08ab57d-6d24-4e2d-849d-9d84840b4b30

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 29 July 2022

Date revision received : 8 September 2022

Date accepted : 13 September 2022

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