2012/07/01 by Wen-Xing Ding, Xiao-Ming Yin · 2 citations
Biochemistry, Genetics and Molecular Biology · Medicine · #Apoptosis #Autophagy #Autophagy in Disease and Therapy #Biochemistry #Biology #Cell biology #Heme Oxygenase-1 and Carbon Monoxide #Medicine #Mitochondrial Function and Pathology #Mitochondrion #Mitophagy #PINK1 #Parkin #Parkinson's disease #Programmed cell death
paper · pdf · doi:10.1515/hsz-2012-0119
openalex publication_date 2012/07/01 · openalex created_date 2016/06/24 · openalex updated_date 2026/08/06
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.