Journal
AGING CELL
Volume 19, Issue 11, Pages -Publisher
WILEY
DOI: 10.1111/acel.13265
Keywords
aging; autophagy; cell‐ nonautonomous; ER stress; protein misfolding; proteostasis
Categories
Funding
- ANID/FONDAP program [15150012]
- Millennium Institute [P09015-F]
- FONDEF [ID16I10223, D11E1007]
- FONDECYT [1180186]
- EcosConicyt [C17S02]
- Michael J Fox For Parkinson's research target validation [12473.01]
- U.S. Office of Naval Research-Global [20RT0419]
- Medical Research Council
- MRC [MC_UP_1201/7] Funding Source: UKRI
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The aging process is characterized by a progressive decline in the function of most tissues, representing the main risk factor in the development of a variety of human diseases. Studies in multiple animal models have demonstrated that interventions that improve the capacity to maintain endoplasmic reticulum (ER) proteostasis prolong life and healthspan. ER stress is monitored by the unfolded protein response (UPR), a signaling pathway that mediates adaptive processes to restore proteostasis or the elimination of damaged cells by apoptosis. Here, we discuss recent advances in understanding the significance of the UPR to aging and its implications for the maintenance of cell physiology of various cell types and organs. The possible benefits of targeting the UPR to extend healthspan and reduce the risk of developing age-related diseases are also discussed.
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