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. 2022 Jul 15;3:926627. doi: 10.3389/fragi.2022.926627

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Copyright © 2022 Tong, Zhang and Wang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mitochondria changes in RPE senescence: PGAM5 dephosphorylates DRP-1 which promotes mitochondrial fission, which then inhibits the increase of ROS and ATP in RPE cellular senescence; H₂O₂ and CSE induce increased mitochondrial ROS and membrane potential, also induce decreased ATP level which cause RPE cellular senescence; PGC-1α is a master regulator of mitochondria biogenesis and could reduce ROS level which may inhibit RPE cellular senescence. PGAM5: phosphoglycerate mutase 5; DRP1: dynamin-related protein 1; H₂O₂: hydrogen peroxide; CSE: cigarette smoke extract; PGC-1α: peroxisome proliferator-activated receptor gamma coactivator-1α; ATP: adenosine triphosphate; ROS: reactive oxygen species; ΔΨm: mitochondrial membrane potential.