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A Year at the Forefront of Proteostasis and Aging

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 ca...

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Detalles Bibliográficos
Autores principales: Thompson, Maximilian A., De-Souza, Evandro A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Company of Biologists Ltd 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9943145/
https://www.ncbi.nlm.nih.gov/pubmed/36794708
http://dx.doi.org/10.1242/bio.059750
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author Thompson, Maximilian A.
De-Souza, Evandro A.
author_facet Thompson, Maximilian A.
De-Souza, Evandro A.
author_sort Thompson, Maximilian A.
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description 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.
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spelling pubmed-99431452023-02-22 A Year at the Forefront of Proteostasis and Aging Thompson, Maximilian A. De-Souza, Evandro A. Biol Open Review 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. The Company of Biologists Ltd 2023-02-16 /pmc/articles/PMC9943145/ /pubmed/36794708 http://dx.doi.org/10.1242/bio.059750 Text en © 2023. Published by The Company of Biologists Ltd https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.
spellingShingle Review
Thompson, Maximilian A.
De-Souza, Evandro A.
A Year at the Forefront of Proteostasis and Aging
title A Year at the Forefront of Proteostasis and Aging
title_full A Year at the Forefront of Proteostasis and Aging
title_fullStr A Year at the Forefront of Proteostasis and Aging
title_full_unstemmed A Year at the Forefront of Proteostasis and Aging
title_short A Year at the Forefront of Proteostasis and Aging
title_sort year at the forefront of proteostasis and aging
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9943145/
https://www.ncbi.nlm.nih.gov/pubmed/36794708
http://dx.doi.org/10.1242/bio.059750
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