Original Contribution  |   July 2020
Novel Dual-Fluorescent Mitophagy Reporter Reveals a Reduced Mitophagy Flux in Type 1 Diabetic Mouse Heart
Author Notes
  • From the Department of Biomedical Sciences at the New York Institute of Technology College of Osteopathic Medicine in Old Westbury (Drs Kobayashi, Huang, and Liang and Mr Patel and Ms Kobayashi); and the Department of Endocrinology at the First Affiliated Hospital of Xi'an Jiaotong University in Xi’ an, China (Dr Zhao). Parts of this study were presented at the 77th and 79th Scientific Sessions of the American Diabetes Association June 2017, San Diego, CA, and June 2019, San Francisco, CA, respectively. 
  • Financial Disclosures: None reported. 
  • Support: This study was supported by a Career Development Grant (1-09-CD-09) from the American Diabetes Association. Dr Liang was supported by grants 1R15HL137130-01A1 and 1R15HL120027-01A1 from the National Institutes of Health. Dr Kobayashi was supported by the Scientist Development Grant (15SDG25080077) from the American Heart Association. 
  •  *Address correspondence to Qiangrong Liang, MD, PhD, New York Institute of Technology College of Osteopathic Medicine, Northern Blvd, PO Box 8000, Old Westbury, NY 11568-8000. Email: qliang03@nyit.edu
     
Article Information
Cardiovascular Disorders / Endocrinology / Diabetes
Original Contribution   |   July 2020
Novel Dual-Fluorescent Mitophagy Reporter Reveals a Reduced Mitophagy Flux in Type 1 Diabetic Mouse Heart
The Journal of the American Osteopathic Association, July 2020, Vol. 120, 446-455. doi:https://doi.org/10.7556/jaoa.2020.072
The Journal of the American Osteopathic Association, July 2020, Vol. 120, 446-455. doi:https://doi.org/10.7556/jaoa.2020.072
Abstract

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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