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Review
. 2023 Feb 15;12(2):bio059750.
doi: 10.1242/bio.059750. Epub 2023 Feb 16.

A Year at the Forefront of Proteostasis and Aging

Affiliations
Review

A Year at the Forefront of Proteostasis and Aging

Maximilian A Thompson et al. Biol Open. .

Abstract

During aging, animals experience a decline in proteostasis activity, including loss of stress-response activation, culminating in the accumulation of misfolded proteins and toxic aggregates, which are causal in the onset of some chronic diseases. Finding genetic and pharmaceutical treatments that can increase organismal proteostasis and lengthen life is an ongoing goal of current research. The regulation of stress responses by cell non-autonomous mechanisms appears to be a potent way to impact organismal healthspan. In this Review, we cover recent findings in the intersection of proteostasis and aging, with a special focus on articles and preprints published between November 2021 and October 2022. A significant number of papers published during this time increased our understanding of how cells communicate with each other during proteotoxic stress. Finally, we also draw attention to emerging datasets that can be explored to generate new hypotheses that explain age-related proteostasis collapse.

Keywords: Cell non-autonomous response; Heat shock response; Longevity; Protein homeostasis; UPR.

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Conflict of interest statement

Competing interests The authors declare no competing or financial interests.

Figures

Fig. 1.
Fig. 1.
Cell non-autonomous regulation of proteostasis and longevity by the nervous system. Both neurons and glia were shown to regulate the HSR, UPRER, and UPRmt in distal tissues in response to genetic interventions or environmental stimulation. This form of signalling depends on the production or secretion of specific neurotransmitters, neuropeptides and other proteins, such as Wnt. Electron Transport Chain (ETC).

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