Autophagy in Mitochondrial Quality Control

  • Rui Wang
  • Guanghui WangEmail author
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 1206)


Autophagy plays an important role in the renewal of cellular components, which function in energy production, metabolism, and clearance of damaged organelles. Both macroautophagy and microautophagy are involved in these processes. Although it was thought that nonselective macroautophagy is responsible for the clearance of damaged or old organelles, recent studies show that the clearance of cellular organelles depends on selective processes. Mitophagy is a process for selective degradation of mitochondria, which is well documented. The selective autophagy for other organelles includes endoplasmic reticulum autophagy (reticulophagy) and peroxisome autophagy (pexophagy). Autophagy is a routine pathway for cells to degrade unused proteins and damaged organelles in cells. Autophagy selectively removes dysfunctional cellular components but not damages the normally functioning organelles, to maintain the homeostasis of cells. In addition to the maintenance of the homeostasis of cells, autophagy clears the damaged organelles in disease or injury conditions to achieve cellular quality control. In some differentiated cells, such as red blood cells, some organelles are removed during the maturation, including mitochondria. The autophagy system can selectively clear the mitochondria and other organelles, which lead to the maturation of red blood cells. Dysfunction of autophagy impairs the clearance of damaged organelles, which results in injury of cells. In the maturation of red blood cells, failure to clear the cellular organelles by autophagy will disturb the normal differentiation of red blood cells, leading to a series of diseases such as anemia.


Autophagy Mitochondria Mitophagy Fission Fusion PINK1 Parkin 



Atg8-family interacting motif


Autophagy-related protein


Carbonyl cyanide m-chlorophenyl hydrazone


Dynamin-related protein 1


Mitochondrial fission 1 protein


Microtubule-associated protein light chain 3


LC3-interacting region




Mitochondrial DNA


Optic atrophy 1




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Copyright information

© Science Press and Springer Nature Singapore Pte Ltd. 2019

Authors and Affiliations

  1. 1.Laboratory of Molecular Neuropathology, Jiangsu Key Laboratory of Neuropsychiatric Diseases & Department of PharmacologyCollege of Pharmaceutical Sciences, Soochow UniversitySuzhouChina

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