Journal
JACC-BASIC TO TRANSLATIONAL SCIENCE
Volume 7, Issue 3, Pages 223-243Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jacbts.2021.12.002
Keywords
cell death; inflammation; mitophagy; TRAF2
Categories
Funding
- National Institutes of Health (NIH) [HL107594]
- Hope Center Viral Vectors Core at Washington University School of Medicine
- Washington University School of Medicine, The Children's Discovery Institute of Washington University
- St. Louis Children's Hospital
- Foundation for Barnes-Jewish Hospital [3770, 4642]
- NIH [HL143431, NS094692]
- Children's Discovery Institute of Washington University [MC-FR2020-919]
- Diabetes Research Center [P30DK020579]
- Nutrition Obesity Research Center at Washington University [P30DK056341]
- St. Louis VA Medical Center
- Pilot and Feasibility grant from the Diabetes Research Center at Washington University (NIDDK) [P30 DK020579]
- Department of Veterans Affairs [I01BX004235]
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Mitophagy plays a critical role in cardiac myocyte function by removing damaged mitochondria and preventing inflammation and cell death to maintain myocardial homeostasis.
Mitochondria are essential for cardiac myocyte function, but damaged mitochondria trigger cardiac myocyte death. Although mitophagy, a lysosomal degradative pathway to remove damaged mitochondria, is robustly active in cardiac myocytes in the unstressed heart, its mechanisms and physiological role remain poorly defined. We discovered a critical role for TRAF2, an innate immunity effector protein with E3 ubiquitin ligase activity, in facilitating physiological cardiac myocyte mitophagy in the adult heart, to prevent inflammation and cell death, and maintain myocardial homeostasis. (J Am Coll Cardiol Basic Trans Science 2022;7:223-243) Published by Elsevier on behalf of the American College of Cardiology Foundation. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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