biostudies-literatureMa XBLRD VANHLBI NIH HHS223-243https://www.ebi.ac.uk/biostudies/studies/S-EPMC8993766biostudies-literatureUnknown7(3)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.JACC. Basic to translational scienceTRAF2, an Innate Immune Sensor, Reciprocally Regulates Mitophagy and Inflammation to Maintain Cardiac Myocyte Homeostasis.PMC8993766I01 BX004235T32 HL007081R01 HL107594I01 BX001969Liu HZhao CQi KRazani BMurphy JTMa XFrench BAKovacs AMargulies KBDiwan ASatoh TMann DLMani KHyrc KIslam MForoughi LJavaheri AEvans SRawnsley DRKumari MfalseTRAF2, an Innate Immune Sensor, Reciprocally Regulates Mitophagy and Inflammation to Maintain Cardiac Myocyte 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.2022-01-01T00:00:00Z2022 Mar2025-04-04T19:10:43.88Z2025-04-04T19:10:43.88ZS-EPMC89937663541132510.1016/j.jacbts.2021.12.002