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Review
. 2017:334:177-205.
doi: 10.1016/bs.ircmb.2017.03.008. Epub 2017 Apr 28.

Senescence-Associated MicroRNAs

Rachel Munk  1 , Amaresh C Panda  1 , Ioannis Grammatikakis  1 , Myriam Gorospe  1 , Kotb Abdelmohsen  2
Affiliations
Review

Senescence-Associated MicroRNAs

Rachel Munk et al. Int Rev Cell Mol Biol. 2017.

Abstract

Senescent cells arise as a consequence of cellular damage and can have either a detrimental or advantageous impact on tissues and organs depending on the specific cell type and metabolic state. As senescent cells accumulate in tissues with advancing age, they have been implicated in many age-related declines and diseases. The major facets of senescence include two pathways responsible for establishing and maintaining a senescence program, p53/CDKN1A(p21) and CDKN2A(p16)/RB, as well as the senescence-associated secretory phenotype. Numerous MicroRNAs influence senescence by modulating the abundance of key senescence regulatory proteins, generally by lowering the stability and/or translation of mRNAs that encode such factors. Accordingly, understanding the molecular mechanisms by which MicroRNAs influence senescence will enable diagnostic and therapeutic opportunities directed at senescent cells. Here, we review senescence-associated (SA)-MicroRNAs and discuss their implications in senescence-relevant pathologies.

Keywords: Age; Aging; MicroRNA; SASP; Senescence; p16; p21; p53.

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Figures

Fig. 1
Fig. 1
SA-MicroRNAs implicated in cellular senescence. Schematic representation of the MicroRNAs that promote or inhibit senescence in three major domains of senescence: the p53/p21 pathway, the p16/RB pathway, and the trait SASP. MicroRNAs that promote senescence are in yellow boxes, MicroRNAs that suppress senescence are in white boxes.
See this image and copyright information in PMC

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