Year: 2026
Type: article
Abstract: Autophagy was originally identified as a survival mechanism to allow cells to survive under nutrient-deprived or stressful conditions whereas cellular senescence was considered a tumor-suppressive mechanism. Both processes can be induced by similar stimuli and can influence each other. There have been continued debates about whether they are causally linked, whether autophagy promotes or prevents senescence or if they are independent of each other. Protein kinases play integral roles in cell fate decision and have a major influence on both autophagy and senescence. While mechanistic target of rapamycin complex 1 is considered the master regulator of autophagy, it also influences senescence. Mitogen-activated protein kinases originally associated with senescence can regulate autophagy. While there have been numerous review articles on the interplay between autophagy and senescence, a comprehensive review on how various kinases participate in this interplay is lacking. The purpose of this review is to learn lessons from some old and recent studies to understand how kinases contribute to this changing field. Since both autophagy and senescence can have beneficial and detrimental effects and kinases are important drug targets, insights regarding how kinases orchestrate these two processes should help develop therapeutic strategies to treat diseases, such as aging and cancer.
Source: Cells
Author: Alakananda Basu
Institution: University of North Texas Health Science Center
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,258
OpenAlex ID: W7166469482