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How do proteins shape our lifespan? Exploring aging at the molecular level
The Biochemist · 2024
Abstract
Aging is a major risk factor for many diseases, including neurodegenerative, diabetes, cancer and cardiovascular diseases. Protein misfolding and consequent aggregation are key pathogenic features of number of age-related disorders. Therefore, correct protein folding and its maintenance are necessary for all cellular health. Proper functional balance of the cellular proteins referred as protein homeostasis (or proteostasis(definition)) is vital for all living cells. Thus, cells maintain protein quality control systems or proteostasis network (PN), which coordinates protein synthesis, folding, and degradation to protect the proteins. However, PN function declines with age, and loss of proteostasis is considered as one of the primary telomere(definition) attrition, cellular senescence(definition))." style="text-decoration:underline dotted; text-underline-offset:2px; cursor:help;">hallmarks of aging(definition). It is not clear whether aging is a cause or consequence of proteostasis decline. Intriguingly, signaling pathways that regulate longevity are also found to modulate the PN. This raises a question whether aging pathways can be targeted to boost proteostasis and extend healthy lifespan. This essay explores the relationship between proteins, aging, and strategies to improve both lifespan and health span.
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- 10.1042/bio_2024_923
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- 2026-10-04 MST
Cite this
APA
Kasturi, P. (2024). How do proteins shape our lifespan? Exploring aging at the molecular level. <em>The Biochemist</em>. https://doi.org/10.1042/bio_2024_923
Vancouver
Kasturi P. How do proteins shape our lifespan? Exploring aging at the molecular level. The Biochemist. 2024. doi:10.1042/bio_2024_923.
BibTeX
@article{prasad2024Howdop,
title = {How do proteins shape our lifespan? Exploring aging at the molecular level},
author = {Prasad Kasturi},
journal = {The Biochemist},
year = {2024},
doi = {10.1042/bio_2024_923},
}
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