Loss of Proteostasis |
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Hallmarks of Aging Miniseries No. 4 Loss of Proteostasis
Over the years, our bodies are subjected to many environmental inputs that put thermal stress, oxidative stress, and osmotic stress on our cells, causing misfolding of proteins. For example, free radicals present in polluted air have been identified as particularly noxious agents in this regard, contributing to multiple aging-related pathologies. In younger cells, micro- and macroautophagy pathways, together with the ubiquitin-proteasome system, take care of clearing these unfolded proteins. However, in aging cells, autophagy induction can be gradually compromised, and lysosomes become less efficient at eliminating the vesicles carrying this cellular waste.
In a vicious cycle termed “inflammaging,” this decrease in efficient autophagy results in an increase in intracellular ROS, triggering the damage-sensing inflammasome to generate low levels of chronic inflammation, further accelerating aging.
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Timecourse imaging of HT-1080 cells after transduction with LentiBrite GFP-LC3 and the addition of a lysosomal inhibitor under starvation conditions. GFP-LC3 displays a diffuse nuclear and cytosolic distribution in fed cells, and a punctate distribution in starved, autophagic cells.| Description | Cat. No. |
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| Hallmarks of Aging |
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