Abstract
Mitochondria are essential organelles that regulate cellular energy homeostasis and cell death. The removal of damaged mitochondria through autophagy, a process called mitophagy, is thus critical for maintaining proper cellular functions. Indeed, mitophagy has been recently proposed to play critical roles in terminal differentiation of red blood cells, paternal mitochondrial degradation, neurodegenerative diseases, and ischemia or drug-induced tissue injury. Removal of damaged mitochondria through autophagy requires two steps: induction of general autophagy and priming of damaged mitochondria for selective autophagic recognition. Recent progress in mitophagy studies reveals that mitochondrial priming is mediated either by the Pink1-Parkin signaling pathway or the mitophagic receptors Nix and Bnip3. In this review, we summarize our current knowledge on the mechanisms of mitophagy. We also discuss the pathophysiological roles of mitophagy and current assays used to monitor mitophagy.
About the authors
Dr. Wen-Xing Ding received his PhD from the National University of Singapore. He is currently an assistant professor at the Department of Pharmacology, Toxicology and Therapeutics at the University of Kansas Medical Center, USA. Dr. Ding’s Lab focuses on the mechanisms of mitophagy in alcohol and drug-induced liver injury. Their ultimate goal is to investigate the possibilities to attenuate alcohol and drug-induced liver injury by modulating autophagy.
Dr. Xiao-Ming Yin, MD, PhD, is a Louis Y. Mazzini Professor of Pathology at the Department of Pathology and Laboratory Medicine, Indiana University School of Medicine. Dr. Yin’s research is centered on the mechanisms of apoptosis and autophagy in tissue injury and cancer therapy.
©2012 by Walter de Gruyter Berlin Boston
