A Futile Battle? Protein Quality Control and the Stress of Aging.

Dev Cell

Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA 94720, USA; The Glenn Center for Aging Research, University of California, Berkeley, Berkeley, CA 94720, USA. Electronic address:

Published: January 2018

AI Article Synopsis

  • Early life stress may actually promote longevity by triggering long-lasting cellular defense mechanisms.
  • The induced pathways include unfolded protein responses in the endoplasmic reticulum, cytosol, and mitochondria.
  • Interestingly, activating these stress responses without any actual stress can extend lifespan in organisms like yeast, worms, and flies.

Article Abstract

There exists a phenomenon in aging research whereby early life stress can have positive impacts on longevity. The mechanisms underlying these observations suggest a robust, long-lasting induction of cellular defense mechanisms. These include the various unfolded protein responses of the endoplasmic reticulum (ER), cytosol, and mitochondria. Indeed, ectopic induction of these pathways, in the absence of stress, is sufficient to increase lifespan in organisms as diverse as yeast, worms, and flies. Here, we provide an overview of the protein quality control mechanisms that operate in the cytosol, mitochondria, and ER and discuss how they affect cellular health and viability during stress and aging.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5896312PMC
http://dx.doi.org/10.1016/j.devcel.2017.12.020DOI Listing

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