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  • Assistant Professor
  • Education:Ph.D., Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan, U.S.A.;Post-doctoral researcher, Center for Autophagy Research, UT-Southwestern Medical Center, Dallas, Texas, U.S.A
  • Office: R506, 5F, Tradition Medicine Building
  • Phone: 886-2-2826-7127
  • Email:


Macroautophagy (hereafter referred to as autophagy) is a catabolic pathway by which cells sequester unwanted or damaged cellular proteins or organelles through a double membrane structure called the autophagosome. This process is mediated by a set of evolutionarily conserved genes, the autophagy-related (ATG) genes, which function in nucleation of the autophagosomal membrane, elongation of the autophagic membrane, sequestration of cytoplasmic constituents, and lysosomal degradation of the sequestered contents.

Selective autophagy is a homeostatic quality control process that targets specific cytoplasmic components to autophagosomes for lysosomal destruction. 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 eliminate damaged or unwanted mitochondria as damaged mitochondria release reactive oxygen species (ROS), leading to inflammasome activation, genotoxic stress, promotion of tumorigenesis and aging. Defects in mitophagy are implicated in neurodegenerative diseases such as Parkinson’s disease, Alzheimer disease, and age-related pathologies. Thus, the proper removal of mitochondria is essential for organismal health in diverse eukaryotic species.

The primary research focus of our laboratory is to understand the molecular regulation and biological functions of mitophagy. A fundamental question in the autophagy field remains how cargos such as mitochondria are selectively targeted for autophagic degradation. We will use series of genetic, cell biology, biochemical approaches to understand the mechanisms that confer substrate selectivity in mitophagy and investigate the pathological consequences of mitophagy dysfunction in diseases using model organisms such as C. elegans and mice. These studies may guide future efforts in developing therapeutic options against age-related and neurodegenerative diseases and pave the way for the development of new treatments for patients with diseases associated with mitochondrial dysfunction.


  • Wei-Chung Chiang, Shuguang Wei, Anwu Zhou, Yi-Chun Kuo, Yongjie Wei, Zhongju Zou, Jenna Yehl, Matthew J. Ranaghan, Adam Skepner, Joshua A. Bittker, Jose R. Perez, Bruce A. Posner and Beth Levine. High Throughput Screens to Identify Autophagy Inducers that Function by Disrupting Beclin 1/Bcl-2 Binding. In review.


  • Álvaro F. Fernández, Salwa Sebti, Yongjie Wei, Zhongju Zou, Mingjun Shi, Kathryn McMillan, Congcong He, Wei-Chung Chiang, Tabitha Ting, Denise Marciano, Gabriele Schiatarella, Govind Bhagat, Orson W. Moe, Ming-Chang Hu and Beth Levine. Disruption of the beclin 1/Bcl-2 autophagy regulatory complex promotes longevity in mice. In review.


  • Yongjie Wei*, Wei-Chung Chiang*, Rhea Sumpter Jr., Prashant Mishra and Beth Levine. Prohibitin 2 is an Inner Mitochondrial Membrane Mitophagy Receptor. Cell. 168(1-2) 224-238 (2017). (*co-first author)


  • Wei-Chung Chiang, Tsui-Ting Ching, Hee-Chul Lee, Carol Mousigian and Ao-Llin Hsu. HSF-1 regulators DDL-1/2 link insulin-like signaling to heat-shock responses and modulation of longevity. Cell. 148(1) 322-334 (2012).


  • Wei-Chung Chiang, Daniel X. Tishkoff, Bo Yang, Joshua Wilson-Grady, Xiaokun Yu, Travis Mazer, Mark Eckersdorff, Steven P. Gygi, David B. Lombard, and Ao-Lin Hsu. C. elegans SIRT6/7 Homolog SIR-2.4 Promotes DAF-16 Relocalization and Function during Stress. PLoS Genetics, 8(9): e1002948.


  • Tsui-Ting Ching, Wei-Chung Chiang, Ching-Shih Chen and Ao-Lin Hsu. Celecoxib Extends Worm Lifespan Independent of COX-2 Inhibition. Aging Cell. 10(3):506-19 (2010).


  • Mu-Hwa Yang, Wei-Chung Chiang, Shyue-Yih Chang, Po-Min Chen and Kou-Juey Wu. Increased NBS1 expression as a prognostic marker of aggressive head and neck cancer and overexpression of NBS1 contributes to transformation. Clin. Cancer Res. 12, 507-515 (2006).


  • Yen-Chung Chen, Yi-Ning Su, Po-Chien Chou, Wei-Chung Chiang, Ming-Cheng Chang, Liang-Shun Wang, Shu-Chun Teng and Kou-Juey Wu. Overexpression of NBS1 contributes to transformation through the activation of phosphatidylinositol 3-kinase/Akt. J. Biol. Chem. 280, 32505-11 (2005).


  • Shih-Hung Yu, Wei-Chung Chiang, Hsiu-Ming Shih and Kou-Juey Wu. Stimulation of c-Rel transcriptional activity by PKA catalytic subunit beta. J. Mol. Med. 82(9):621-8 (2004).


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