Moderately cold temperatures trigger the removal of aggregation-prone proteins in the invertebrate model Caenorhabditis elegans and cultured human cells, preventing the accumulation of pathological aggregates linked with age-related neurodegenerative disorders such as amyotrophic lateral sclerosis and Huntington’s disease.
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References
López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M. & Kroemer, G. Hallmarks of aging: an expanding universe. Cell 186, 243–278 (2023). A review that presents twelve hallmarks of aging, including loss of proteostasis.
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Lee, H. J. et al. Prostaglandin signals from adult germline stem cells delay somatic ageing of Caenorhabditis elegans. Nat. Metab. 1, 790–810 (2019). This paper reports that cold temperature coordinates extended reproductive capacity with somatic fitness.
Xiao, R. et al. A genetic program promotes C. elegans longevity at cold temperatures via a thermosensitive TRP channel. Cell 152, 806–817 (2013). This paper reports that the TRPA1 channel detects low temperature to extend lifespan, demonstrating that genetics programs contribute to cold-induced longevity.
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This is a summary of: Lee, H. J. et al. Cold temperature extends longevity and prevents disease-related protein aggregation through PA28γ-induced proteasomes. Nat. Aging https://doi.org/10.1038/s43587-023-00383-4 (2023).
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Moderately cold temperatures prevent protein aggregation related to aging and disease. Nat Aging 3, 479–480 (2023). https://doi.org/10.1038/s43587-023-00397-y
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DOI: https://doi.org/10.1038/s43587-023-00397-y
