Mastering organismal aging through the endoplasmic reticulum proteostasis network

Taylor, Rebecca C. ORCID: https://orcid.org/0000-0003-3429-3123 and Hetz, Claudio (2020) Mastering organismal aging through the endoplasmic reticulum proteostasis network. Aging Cell, 19 (11). ISSN 1474-9718

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Abstract

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.

Item Type: Article
Additional Information: Author acknowledgements: We thank Dr Hery Urra for figure design. ANID/FONDAP program 15150012, Millennium Institute P09‐015‐F, CONICYT‐Brazil 441921/2016‐7, FONDEF ID16I10223, FONDEF D11E1007, and FONDECYT 1180186 and Ecos‐Conicyt no. C17S02 (CH). In addition, we thank the support from the U.S. Air Force Office of Scientific Research 20RT0419, and Michael J Fox For Parkinson's research target validation ID 12473.01 (CH), U.S. Funding was also provided by the Medical Research Council (RT).
Uncontrolled Keywords: aging,autophagy,cell-nonautonomous,er stress,protein misfolding,proteostasis,ageing,cell biology,sdg 3 - good health and well-being ,/dk/atira/pure/subjectarea/asjc/1300/1302
Faculty \ School: Faculty of Science > School of Biological Sciences
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Depositing User: LivePure Connector
Date Deposited: 16 Jan 2023 17:32
Last Modified: 23 Jan 2023 10:30
URI: https://ueaeprints.uea.ac.uk/id/eprint/90605
DOI: 10.1111/acel.13265

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