Chiang Wei-Chung

Selective autophagy is a homeostatic quality control process that targets specific cytoplasmic components to autophagosomes, ultimately resulting in their destruction in the lysosome. Diverse cargos have been identified as substrates for selective autophagy, including mitochondria (mitophagy), peroxisomes (pexophagy), endoplasmic reticulum (ERophagy), and viruses (virophagy). Mitophagy is the major pathway by which eukaryotic cells target damaged or unwanted mitochondria for lysosomal destruction. Damaged mitochondria release reactive oxygen species (ROS), leading to inflammasome activation, genotoxic stress, promotion of tumorigenesis and aging. Defects in mitophagy likely contribute to neurodegenerative diseases, inflammatory diseases, cancer and decreased lifespan. Thus, the proper removal of mitochondria is essential for organismal health in diverse eukaryotic species My research focus is to understand the molecular regulation and physiological functions of selective autophagy. A fundamental question in the autophagy field remains how cargos are selectively targeted for autophagic degradation. I am interested in understanding the mechanisms that confer substrate selectivity in mitophagy and in investigating the pathological consequences of mitophagy dysfunction in human diseases. My laboratory use a combination of biochemical, cell biological, and genetic approaches to delineate the molecular regulation and physiological functions of mitophagy. I expect that these studies will not only yield a better fundamental understanding of mitophagy but also result in novel therapeutic options for aging and human diseases.