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. 2020 May 26;11:755. doi: 10.3389/fphar.2020.00755

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Copyright © 2020 Docherty, Baird, Hughes and Ferenbach

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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Putative roles for senescent cells in the evolution of maladaptive repair after acute kidney injury. Our understanding of the role of senescence in the evolution of maladaptive repair after injury remains incomplete. Evidence from clinical studies identifies increasing numbers of senescent cells in the aged and chronically damaged kidney, and experimental models show reduced renal fibrosis after senolytic treatments. In this diagram, we outline potential mechanisms by which senescent cells generated in response to aging or injury may promote ongoing fibrosis via SASP release leading to immune activation, fibroblast proliferation, and further induction of paracrine senescence.