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. 2021 Nov 25;9:714320. doi: 10.3389/fcell.2021.714320

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Copyright © 2021 Wu, Liang, Li, Wen, Tang and Liu.

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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G2/M phase arrest of TECs mediates renal fibrosis by secreting profibrotic cytokines. Injuries result in the activation of ATM/ATR, which could promote the activation of Chk1/Chk2 and p53. p53 and Chk1/Chk2 could induce downregulation of Cdk1/cyclin B kinase activity by affecting p21 and Cdc25, respectively. The downregulation of Cdk1/cyclin B kinase activity results in TECs G2/M phase arrest; the arrested cells undergo senescence and manifest senescence-associated secretory phenotype (SASP), causing renal fibrosis by secreting profibrotic cytokines, such as TGF-β1 and CTGF.