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Mitophagy is the selective degradation of mitochondria by autophagy.It often occurs to defective mitochondria following damage or stress. The process of mitophagy was first described in 1915 by Margaret Reed Lewis and Warren Harmon Lewis. [1]
In the selective autophagy is the autophagy of organelles; mitophagy, [36] lipophagy, [37] pexophagy, [38] chlorophagy, [39] ribophagy [40] and others. Macroautophagy is the main pathway, used primarily to eradicate damaged cell organelles or unused proteins . [ 41 ]
MAP1LC3B is a member of the highly conserved ATG8 protein family. ATG8 proteins are present in all known eukaryotic organisms. The animal ATG8 family comprises three subfamilies: (i) microtubule-associated protein 1 light chain 3 (MAP1LC3); (ii) Golgi-associated ATPase enhancer of 16 kDa (GATE-16); and (iii) γ-amino-butyric acid receptor-associate protein ().
Atg8 is one of the key molecular components involved in autophagy, the cellular process mediating the lysosome/vacuole-dependent turnover of macromolecules and organelles. [5] Autophagy is induced upon nutrient depletion or rapamycin treatment and leads to the response of more than 30 autophagy-related (ATG) genes known so far, including ATG8.
Atg1 is a kinase upregulated upon induction of autophagy. Atg13 regulates Atg1 and together they form a complex called Atg13:Atg1, which receives signals from the master of nutrient sensing – Tor. Atg1 is also important in late stages of autophagosome formation. [8]
Myopathies involving abnormal autophagy, including abnormal mitophagy, may present with secondary impaired fatty acid metabolism and/or mitochondrial defects in skeletal muscles, may have wide phenotypic variability, and may affect multiple other organs.
Autophagy protein 5 (ATG5) is a protein that, in humans, is encoded by the ATG5 gene located on chromosome 6. It is an E3 ubi autophagic cell death. ATG5 is a key protein involved in the extension of the phagophoric membrane in autophagic vesicles. It is activated by ATG7 and forms a complex with ATG12 and ATG16L1.
Mitophagy is the elimination of damaged mitochondria in autophagosomes, and is dependent on a positive feedback cycle involving synergistic action of parkin and PINK1. Following severe cellular insult, rundown of mitochondrial membrane potential prevents import of PINK1 into the mitochondrial matrix and causes it to aggregate on the outer ...