Mitochondria in cell senescence: A Friend or Foe?

Document Type

Article

Publication Date

1-1-2023

Abstract

Cell senescence denotes cell growth arrest in response to continuous replication or stresses damaging DNA or mitochondria. Mounting research suggests that cell senescence attributes to aging-associated failing organ function and diseases. Conversely, it participates in embryonic tissue maturation, wound healing, tissue regeneration, and tumor suppression. The acute or chronic properties and microenvironment may explain the double faces of senescence. Senescent cells display unique characteristics. In particular, its mitochondria become elongated with altered metabolomes and dynamics. Accordingly, mitochondria reform their function to produce more reactive oxygen species at the cost of low ATP production. Meanwhile, destructed mitochondrial unfolded protein responses further break the delicate proteostasis fostering mitochondrial dysfunction. Additionally, the release of mitochondrial damage-associated molecular patterns, mitochondrial Ca

Publication Title

Advances in Protein Chemistry and Structural Biology

Volume

136

First Page

35

Last Page

91

PubMed ID

37437984

Comments

This article was published in Advances in Protein Chemistry and Structural Biology, Volume 136.

The published version is available at https://doi.org/10.1016/bs.apcsb.2023.02.019.

Copyright © 2023. Published by Elsevier Inc.

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