1)School of Clinical Medicine, Changchun University of Chinese Medicine, Changchun 130021, China;2)Diagnostic Medical Research Center, Jilin Provincial People’s Hospital, Changchun 130021, China;3)School of Medical Laboratory Science, Beihua University, Jilin 132013, China;4)School of Life Sciences, Changchun Normal University, Changchun 130123, China
This work was surported by grants from The National Natural Science Foundation of China (31900823, 32011540004), Jilin Talents Developing Fund (2019019) and Health Commission of Jilin Province (2019J069).
Mitochondria is an major organelle for cellular physiology and metabolism. The homeostasis of mitochondrial biogenesis and degradation is important in maintaining the stability of energy metabolism. Mitophagy is regulated by PINK1/Parkin and LC3 signaling. Parkin, as an E3 ubiquitin ligase, mediates the process of mitochondrial degradation. Parkin is also involved in many other intracellular metabolic activities, such as regulating mitochondrial associated membrane (MAM) and controlling calcium flow in-between organelles. In response to external stimuli like chronic cold exposure, with abundant mitochondria biogenesis, beige adipocytes are generated in the white adipose tissue. Following the withdrawal of external stimuli, beige adipocytes directly acquire a white fat-like phenotype. Beige adipocyte is an ideal model to study the mechanism of mitochondrial regulation. However, the regulatory mechanism of mitochondrial homeostasis is still unclear. We have reviewed recent studies of novel mechanism on Parkin-mediated mitophagy, and furthermore, the regulatory mechanisms of organelle contacts between mitochondria, endoplasmic reticulum and lysosome.
ZHANG Xiao-Fang, LI Si-Qi, ZHANG Qiang, ZHANG Jing, LU Xiao-Dan. Parkin-mediated Mitophagy and Organelle Contacts[J]. Progress in Biochemistry and Biophysics,2021,48(11):1253-1259
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