期刊
JOURNAL OF THE AMERICAN OSTEOPATHIC ASSOCIATION
卷 120, 期 7, 页码 446-455出版社
AMER OSTEOPATHIC ASSN
DOI: 10.7556/jaoa.2020.072
关键词
diabetes; diabetic cardiomyopathy; mitochondria; mitophagy
资金
- American Diabetes Association [1-09-CD-09]
- National Institutes of Health [1R15HL137130-01A1, 1R15HL120027-01A1]
- American Heart Association [15SDG25080077]
Context: Patients with diabetes are susceptible to heart failure. Defective mitochondria can cause cardiac damage. Mitochondrial autophagy or mitophagy is a quality control mechanism that eliminates dysfunctional mitochondria through lysosome degradation. Mitophagy is essential for maintaining a pool of healthy mitochondria for normal cardiac function. However, the effect of diabetes on the functional status of cardiac mitophagy remains unclear. Objective: To determine and compare cardiac mitophagy flux between diabetic and nondiabetic mice. Methods: Using a novel dual fluorescent mitophagy reporter termed mt-Rosella, we labeled and traced mitochondrial fragments that are sequestered by the autophagosome and delivered to and degraded in the lysosome. Results: Mitophagic activity was reduced in high-glucose- treated cardiomyocytes and in the heart tissue of type 1 diabetic mice. Conclusions: Mitophagy was impaired in the heart of diabetic mice, suggesting that restoring or accelerating mitophagy flux may be a useful strategy to reduce cardiac injury caused by diabetes.
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