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Full-coverage regulations of autophagy by ROS: from induction to maturation
Zhou, Jing1,2; Li, Xin Yu1; Liu, Yu Jia1; Feng, Ji3; Wu, Yong3; Shen, Han Ming2,4; Lu, Guo Dong1,3
Source PublicationAutophagy

Macroautophagy/autophagy is an evolutionarily well-conserved recycling process in response to stress conditions, including a burst of reactive oxygen species (ROS) production. High level of ROS attack key cellular macromolecules. Protein cysteinyl thiols or non-protein thiols as the major redox-sensitive targets thus constitute the first-line defense. Autophagy is unique, because it removes not only oxidized/damaged proteins but also bulky ROS-generating organelles (such as mitochondria and peroxisome) to restrict further ROS production. The oxidative regulations of autophagy occur in all processes of autophagy, from induction, phagophore nucleation, phagophore expansion, autophagosome maturation, cargo delivery to the lysosome, and finally to degradation of the cargo and recycling of the products, as well as autophagy gene transcription. Mechanically, these regulations are achieved through direct or indirect manners. Direct thiol oxidation of key proteins such as ATG4, ATM and TFEB are responsible for specific regulations in phagophore expansion, cargo recognition and autophagy gene transcription, respectively. Meanwhile, oxidation of certain redox-sensitive chaperone-like proteins (e.g. PRDX family members and PARK7) may impair a nonspecifically local reducing environment in the phagophore membrane, and influence BECN1-involved phagophore nucleation and mitophagy recognition. However, ROS do exhibit some inhibitory effects on autophagy through direct oxidation of key autophagy regulators such as ATG3, ATG7 and SENP3 proteins. SQSTM1 provides an alternative antioxidant mechanism when autophagy is unavailable or impaired. However, it is yet to be unraveled how cells evolve to equip proteins with different redox susceptibility and in their correct subcellular positions, and how cells fine-tune autophagy machinery in response to different levels of ROS. Abbreviations: AKT1/PKB: AKT serine/threonine kinase 1; AMPK: AMP-activated protein kinase; ATG: autophagy related; ATM: ATM serine/threonine kinase; BAX: BCL2 associated X, apoptosis regulator; BECN1: beclin 1; BH3: BCL2-homology-3; CAV1: caveolin 1; CCCP: carbonyl cyanide m-chlorophenylhydrazone; CTSB: cathepsin B; CTSL: cathepsin L; DAPK: death associated protein kinase; ER: endoplasmic reticulum; ETC: electron transport chain; GSH: glutathione; GSTP1: glutathione S-transferase pi 1; HO: hydrogen peroxide; HK2: hexokinase 2; KEAP1: kelch like ECH associated protein 1; MAMs: mitochondria-associated ER membranes; MAP1LC3B/LC3: microtubule associated protein 1 light chain 3 beta; MAPK8/JNK1: mitogen-activated protein kinase 8; MAP3K5/ASK1: mitogen-activated protein kinase kinase kinase 5; MCOLN1: mucolipin 1; MMP: mitochondrial membrane potential; MTOR: mechanistic target of rapamycin kinase; NFE2L2/NRF2: nuclear factor, erythroid 2 like 2; NFKB1: nuclear factor kappa B subunit 1; NOX: NADPH oxidase; O: superoxide radical anion; p-Ub: phosphorylated Ub; PARK7/DJ-1: Parkinsonism associated deglycase; PE: phosphatidylethanolamine; PEX5: peroxisomal biogenesis factor 5; PINK1: PTEN induced kinase 1; PPP3CA/calcineurin: protein phosphatase 3 catalytic subunit beta; PRDX: peroxiredoxin; PRKAA1: protein kinase AMP-activated catalytic subunit alpha 1; PRKD/PKD: protein kinase D; PRKN/parkin: parkin RBR E3 ubiquitin protein ligase; PtdIns3K: class III phosphatidylinositol 3-kinase; PtdIns3P: phosphatidylinositol-3-phosphate; PTEN: phosphatase and tensin homolog; ROS: reactive oxygen species; SENP3: SUMO specific peptidase 3; SIRT1: sirtuin 1; SOD1: superoxide dismutase 1; SQSTM1/p62: sequestosome 1; SUMO: small ubiquitin like modifier; TFEB: transcription factor EB; TRAF6: TNF receptor associated factor 6; TSC2: TSC complex subunit 2; TXN: thioredoxin; TXNRD1: thioredoxin reductase 1; TXNIP: thioredoxin interacting protein; Ub: ubiquitin; ULK1: unc-51 like autophagy activating kinase 1.

KeywordAtgs Autophagy Oxidative Regulation Protein Thiols Ros
URLView the original
Indexed BySCIE
WOS Research AreaCell Biology
WOS IDWOS:000707823500001
Scopus ID2-s2.0-85117180477
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Cited Times [WOS]:16   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionFaculty of Health Sciences
Corresponding AuthorShen, Han Ming; Lu, Guo Dong
Affiliation1.Department of Physiology, School of Preclinical Medicine, Guangxi Medical University, Nanning, Guangxi Province, China
2.Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
3.Department of Toxicology, School of Public Health, Guangxi Medical University, Nanning, Guangxi Province, China
4.Faculty of Health Sciences, University of Macau, Macau, China
Corresponding Author AffilicationFaculty of Health Sciences
Recommended Citation
GB/T 7714
Zhou, Jing,Li, Xin Yu,Liu, Yu Jia,et al. Full-coverage regulations of autophagy by ROS: from induction to maturation[J]. Autophagy,2021.
APA Zhou, Jing,Li, Xin Yu,Liu, Yu Jia,Feng, Ji,Wu, Yong,Shen, Han Ming,&Lu, Guo Dong.(2021).Full-coverage regulations of autophagy by ROS: from induction to maturation.Autophagy.
MLA Zhou, Jing,et al."Full-coverage regulations of autophagy by ROS: from induction to maturation".Autophagy (2021).
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