title: Myocardial redox status, mitophagy and cardioprotection: a potential way to amend diabetic heart?
abstract: Diabetic cardiomyopathy (DCM) is one of the major cardiovascular complications in diabetes that increase the mortality of diabetic patients. Mechanisms underlying DCM have not been fully elucidated, hindering targeted design of effective strategies to delay or treat DCM. Mitochondrial dysfunction is recognized as the driving force for the pathogenesis of DCM; therefore, maintaining cardiac mitochondrial quality is crucial for DCM prevention. Mitophagy is the process by which cells degrade abnormal or superfluous mitochondria in order to correct mitochondrial dysfunction, improve mitochondrial quality and maintain cardiac homoeostasis. Although the roles of mitophagy in various cardiomyopathies have been suggested, it remains largely unknown how the process is regulated and whether it is altered in the diabetic heart. In this review, we summarize currently available studies that investigate mitophagy in the heart, including its pathways, features and protective roles in several situations, including DCM. Due to limited data about mitophagy in diabetic hearts, future studies are required to gain a deeper understanding of the regulatory mechanisms of mitophagy in the heart and to develop mitophagy-based strategies for protecting the heart from diabetic injury.
authors.affiliation: Departments of Cardiovascular Center and Geriatric Medicine, the first Hospital of Jilin University, Changchun 130021, China Kosair Children's Hospital Research Institute, the Departments of Pediatrics, Radiation Oncology, the University of Louisville, Louisville, KY 40202, U.S.A.
authors.forename: Tao
authors.initials: T
authors.lastname: Bai
authors.affiliation: Department of Internal Medicine, People's Hospital of Jilin Province, Changchun 130021, Jilin, China.
authors.forename: Fan
authors.initials: F
authors.lastname: Wang
authors.affiliation: Departments of Cardiovascular Center and Geriatric Medicine, the first Hospital of Jilin University, Changchun 130021, China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Zheng
authors.affiliation: Department of Biomedical Sciences, New York Institute of Technology College of Osteopathic Medicine, Old Westbury, NY 11568, U.S.A.
authors.forename: Qiangrong
authors.initials: Q
authors.lastname: Liang
authors.affiliation: Departments of Cardiovascular Center and Geriatric Medicine, the first Hospital of Jilin University, Changchun 130021, China.
authors.forename: Yuehui
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Departments of Cardiovascular Center and Geriatric Medicine, the first Hospital of Jilin University, Changchun 130021, China kongjian-2005@163.com l0cai001@louisville.edu.
authors.forename: Jian
authors.initials: J
authors.lastname: Kong
authors.affiliation: Kosair Children's Hospital Research Institute, the Departments of Pediatrics, Radiation Oncology, the University of Louisville, Louisville, KY 40202, U.S.A. kongjian-2005@163.com l0cai001@louisville.edu.
authors.forename: Lu
authors.initials: L
authors.lastname: Cai
mesh_terms: D000818:Animals; D058065:Diabetic Cardiomyopathies / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D006321:Heart / Q000503:physiopathology; D006801:Humans; D008928:Mitochondria / Q000502:physiology*; D063306:Mitophagy; D009206:Myocardium / Q000378:metabolism*; D010084:Oxidation-Reduction
keywords: diabetic cardiomyopathy; mitochondrial dysfunction; mitochondrial quality control; mitophagy; redox