Why do cells, and therefore humans, age? The answer may have a lot to do with mitochondria, the organelles that power cells. The idea is not new, but direct evidence in human cells has so far been lacking. until now.
In a study published on January 12, communication biology, A team led by researchers from Columbia University found that human cells with damaged mitochondria respond by gearing up and expending more energy. This adaptation, called hypermetabolism, enhances short-term cell viability, but at a high cost. That is, the rate of cellular aging increases dramatically.
“The findings were made in cells from patients with rare mitochondrial diseases, but may also be relevant to other conditions that affect mitochondria, such as neurodegenerative diseases, inflammatory conditions and infections.” , said principal investigator and associate professor of behavioral science Dr. Martin Picard. He graduated from Columbia University’s Vagelos College of Physicians and Surgeons in Medicine (Psychiatry and Neurology).
“Furthermore, hypermetabolism may be the main reason why most cells deteriorate with age.”
Hypermetabolic cells age faster
It was generally believed that mitochondrial defects (impaired conversion of food sources into usable energy) slowed the metabolic rate of cells in order to conserve energy. and energy expenditure, they found that cells with damaged mitochondria doubled their energy expenditure. Furthermore, a reanalysis of data from hundreds of patients with various mitochondrial diseases showed that mitochondrial defects also increased energy costs at the systemic level.
This energy boost keeps cells moving, but also breaks down their telomeres (caps that protect the ends of chromosomes) and activates the stress response and inflammation. The net effect is to accelerate biological aging.
“When cells expend more energy to make proteins and other substances essential for short-term survival, they may be stealing resources from processes that ensure long-term survival, such as maintaining telomeres.” the study.
Hypermetabolism, Fatigue, Aging
This hypermetabolic state may explain why patients with mitochondrial disease experience fatigue and exercise intolerance, among other symptoms. It ‘tells’ you to conserve energy, not to over-exercise. We are likely to see the same dynamics as people age and lose energy,” Picard said. say.
While the study does not represent a new treatment for patients with currently untreatable mitochondrial disease, it does strengthen current recommendations for patients to move more. Maybe, because being more active can expend more energy and make symptoms worse,” says Sturm. “However, exercise is known to increase the efficiency of the organism. For example, a person who runs uses less energy to maintain basic bodily processes than a person who is physically inactive.” increase.”
Improved bioefficiency, which reduces intracellular energy expenditure and ameliorate fatigue and other symptoms, may partially explain the health benefits of exercise in patients with mitochondrial diseases and other healthy people.
When looking for new treatments for mitochondrial diseases, researchers should focus on hypermetabolism, says Picard. “Although mitochondrial defects impair a cell’s ability to produce energy, energy deficiency may not be the primary disease initiator. Our study suggests that these defects increase energy expenditure.” We may need to target hypermetabolism to move the needle therapeutically, and more research is needed to know if it works.”
Hypermetabolism is also common in other diseases. If increased cellular energy expenditure is responsible for accelerating the aging process, targeting hypermetabolism could be a way to ameliorate fatigue, improve people’s quality of life, and even slow biological aging. There is a possibility.
This study was supported by the National Institutes of Health (R01AG066828), the Baszucki Brain Research Fund, the J. Willard and Alice S. Marriott Foundation, the Muscular Dystrophy Association, the Nicholas Nunno Foundation, the JDF Fund for Mitochondrial Research, and the Schumann Mitochondrial Diseases Fund.