Mitochondrial quality control in cardiac cells: Mechanisms and role in cardiac cell injury and disease

• Published in: Journal of cellular physiology Vol. 234; no. 6; pp. 8122 - 8133
• Main Authors: Tahrir, Farzaneh G., Langford, Dianne, Amini, Shohreh, Mohseni Ahooyi, Taha, Khalili, Kamel
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01-06-2019
• Subjects: bcl‐2‐associated athanogene 3 (BAG3); Bioenergetics; cardiomyopathy; Cardiovascular diseases; Cardiovascular Diseases - genetics; Cardiovascular Diseases - metabolism; Cardiovascular Diseases - pathology; Cell injury; Congestive heart failure; Contraction; Coronary artery disease; Coupling (molecular); Disease control; fission; fusion; Heart Injuries - genetics; Heart Injuries - metabolism; Heart Injuries - pathology; Homeostasis; Humans; ischemia/reperfusion (IR) injury; Mitochondria; Mitochondria, Heart - genetics; Mitochondria, Heart - metabolism; Mitochondria, Heart - pathology; Mitochondrial Dynamics - genetics; Mitochondrial Proteins - genetics; mitochondrial quality control; mitophagy; Mitophagy - genetics; Myocardial infarction; Myocytes, Cardiac - metabolism; Myocytes, Cardiac - pathology; Oxidative phosphorylation; Pathogenesis; Phosphorylation; proteasome; Proteins; Quality control; Reactive oxygen species; Reactive Oxygen Species - metabolism; fusion; mitochondrial quality control; proteasome; mitophagy; ischemia/reperfusion (IR) injury; fission; bcl-2-associated athanogene 3 (BAG3); cardiomyopathy
• ISSN: 0021-9541; 1097-4652
• DOI: 10.1002/jcp.27597

Mitochondria play an important role in maintaining cardiac homeostasis by supplying the major energy required for cardiac excitation–contraction coupling as well as controlling the key intracellular survival and death pathways. Healthy mitochondria generate ATP molecules through an aerobic process known as oxidative phosphorylation (OXPHOS). Mitochondrial injury during myocardial infarction (MI) impairs OXPHOS and results in the excessive production of reactive oxygen species (ROS), bioenergetic insufficiency, and contributes to the development of cardiovascular diseases. Therefore, mitochondrial biogenesis along with proper mitochondrial quality control machinery, which removes unhealthy mitochondria is pivotal for mitochondrial homeostasis and cardiac health. Upon damage to the mitochondrial network, mitochondrial quality control components are recruited to segregate the unhealthy mitochondria and target aberrant mitochondrial proteins for degradation and elimination. Impairment of mitochondrial quality control and accumulation of abnormal mitochondria have been reported in the pathogenesis of various cardiac disorders and heart failure. Here, we provide an overview of the recent studies describing various mechanistic pathways underlying mitochondrial homeostasis with the main focus on cardiac cells. In addition, this review demonstrates the potential effects of mitochondrial quality control dysregulation in the development of cardiovascular disease.
Parkin‐mediated mitophagy in Drosophila heart. (a) Parkin deficiency in Drosophila heart impaired mitophagy and led to the development of dilated cardiomyopathy. (b) Simultaneous deletion of mitochondrial assembly regulatory factor and Parkin rescued cardiomyopathy (Bhandari et al., ).