Senescence-Inflammatory Regulation of Reparative Cellular Reprogramming in Aging and Cancer

Frontiers in Cell and Developmental Biology
Javier A Menendez, Tomás Alarcón

Abstract

The inability of adult tissues to transitorily generate cells with functional stem cell-like properties is a major obstacle to tissue self-repair. Nuclear reprogramming-like phenomena that induce a transient acquisition of epigenetic plasticity and phenotype malleability may constitute a reparative route through which human tissues respond to injury, stress, and disease. However, tissue rejuvenation should involve not only the transient epigenetic reprogramming of differentiated cells, but also the committed re-acquisition of the original or alternative committed cell fate. Chronic or unrestrained epigenetic plasticity would drive aging phenotypes by impairing the repair or the replacement of damaged cells; such uncontrolled phenomena of in vivo reprogramming might also generate cancer-like cellular states. We herein propose that the ability of senescence-associated inflammatory signaling to regulate in vivo reprogramming cycles of tissue repair outlines a threshold model of aging and cancer. The degree of senescence/inflammation-associated deviation from the homeostatic state may delineate a type of thresholding algorithm distinguishing beneficial from deleterious effects of in vivo reprogramming. First, transient activation o...Continue Reading

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Citations

Mar 16, 2018·PLoS Computational Biology·Núria Folguera-BlascoTomás Alarcón
Oct 3, 2017·Aging and Disease·William C Cho
Jun 12, 2018·Cell Cycle·Elisabet CuyàsJavier A Menendez
May 1, 2019·PLoS Computational Biology·Núria Folguera-BlascoTomás Alarcón
Aug 25, 2019·Aging·Javier A MenendezTomás Alarcón
May 15, 2018·Frontiers in Cardiovascular Medicine·Fabiana Passaro, Gianluca Testa
Aug 18, 2021·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Sajjad AshrafRita Kandel

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Methods Mentioned

BETA
environmental stresses

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