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Biochim Biophys Acta. 2015 Feb;1852(2):252-61. doi: 10.1016/j.bbadis.2014.05.020. Epub 2014 May 29.

Autophagy and mitophagy in diabetic cardiomyopathy.

Author information

1
Department of Biomedical Sciences, New York Institute of Technology College of Osteopathic Medicine, Old Westbury, NY, USA.
2
Department of Biomedical Sciences, New York Institute of Technology College of Osteopathic Medicine, Old Westbury, NY, USA. Electronic address: qliang03@nyit.edu.

Abstract

Diabetic cardiomyopathy is a heart muscle-specific disease that increases the risk of heart failure and mortality in diabetic patients independent of vascular pathology. Mitochondria are cellular power plants that generate energy for heart contraction and concurrently produce reactive oxygen species that, if unchecked, may damage the mitochondria and the heart. Elimination of damaged mitochondria by autophagy known as mitophagy is an essential process for maintaining normal cardiac function at baseline and in response to various stress and disease conditions. Mitochondrial structural injury and functional impairment have been shown to contribute to diabetic heart disease. Recent studies have demonstrated an inhibited autophagic flux in the hearts of diabetic animals. Surprisingly, the diminished autophagy appears to be an adaptive response that protects against cardiac injury in type 1 diabetes. This raises several questions regarding the relationship between general autophagy and selective mitophagy in the diabetic heart. However, autophagy may play a different role in the hearts of type 2 diabetic animals. In this review, we will summarize current knowledge in this field and discuss the potential functional roles of autophagy and mitophagy in the pathogenesis of diabetic cardiomyopathy. This article is part of a Special Issue entitled: Autophagy and protein quality control in cardiometabolic diseases.

KEYWORDS:

Autophagy; Diabetes; Diabetic cardiomyopathy; Mitochondrion; Mitophagy

PMID:
24882754
DOI:
10.1016/j.bbadis.2014.05.020
[Indexed for MEDLINE]
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