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A little stress can be good for cellular health, find molecular biologists.
The work will help researchers better understand the molecular mechanisms that drive aging and risk for age-associated degenerative diseases.
In a genetic study of the transparent roundworm C. elegans, the research team found that signals from mildly stressed mitochondria (the cellular source of energy) prevent the failure of protein-folding quality-control (proteostasis) machinery in the cytoplasm that comes with age.
This, in turn, suppresses the accumulation of damaged proteins that can occur in degenerative diseases, such as Alzheimer’s, Huntington’s, and Parkinson’s diseases and amyotrophic lateral sclerosis (ALS).
“I never would have guessed this—a low stress signal resets the organismal lifespan profoundly.”
“This has not been seen before,” says Richard I. Morimoto, the senior author of the study, professor of molecular biosciences, and director of the Rice Institute for Biomedical Research at Northwestern University.
“People have always known that prolonged mitochondrial stress can be deleterious. But we discovered that when you stress mitochondria just a little, the mitochondrial stress signal is actually interpreted by the cell and animal as a survival strategy. It makes the animals completely stress-resistant and doubles their lifespan. It’s like magic.”
C. elegans has a biochemical environment and cellular properties similar to that of humans and is a popular research tool for studying the biology of aging and as a model of human disease. Components identified by scientists as playing a role in biological aging are conserved in all animals, including humans, and offer targets for future study.