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Mitochondria Aging Anti-Aging Research Science Cellular Reprogramming

Tackling Cellular Aging

4 months, 2 weeks ago

4190  0
Posted on Feb 25, 2020, 6 p.m.

Mitochondria have been discovered to trigger senescence through communication with the cell’s nucleus, and an FDA approved drug has been revealed to help suppress the damaging effects of the condition in animal studies. Findings published in Genes & Development are hoped to eventually lead to treatments that may promote healthy aging and prevent age related diseases.

"Our findings provide a foundation upon which we can start to develop drugs that extend our health span -- the number of years we live a healthy life," says Peter Adams, Ph.D., a professor in Sanford Burnham Prebys' National Cancer Institute (NCI)-designated Cancer Center and senior author of the study. "Given the major social and economic hurdles we will soon face as millions of Americans grow older, interventions can't come soon enough."

By 2060 the number of people in America who will be aged 65 or older is projected to more than double to reach an estimated 90 million, which will represent close to 25% of the population. Currently close to 80% of all adults have at least two chronic diseases such as diabetes, cancer, or heart disease. The projected increase highlights the need to solve the health problems we face today before a wave hits us, these projections are fueling scientists to search the molecular causes of aging to find the interventions that will help people live longer and healthier lives. 

"To cope with the rise of chronic diseases from an aging population, we must understand the fundamental biological effects of aging," says Mark R. Collins, president and director of the Glenn Foundation, which partially funded the research. "These findings provide insights that bring us closer to treatment(s) that could prevent or delay the onset of many age-related diseases."

Adams has been studying how clusters of chromatin leak out to the cytoplasm in senescent cells to trigger inflammatory signals that promote a variety of undesirable health conditions. This study was designed to investigate what prompts the formation of chromatin clusters to begin with. A series of experiments were conducted using human cell models of senescence, which revealed that mitochondria were driving the formation of proinflammatory cytoplastic chromatin via a retrograde communication path to the nucleus. 

"In school we learned that the role of mitochondria is to generate energy -- and that DNA controls everything the cell does," says Adams. "Research is now showing that mitochondria are important sensors for the cell and have a lot of cross-talk with the nucleus, which makes sense given their duty to respond to the cell's metabolic needs."

An FDA approved HDAC inhibitor was found to transform senescent cells from being large and flat formed into a healthier and more visually youthful state; and the treated cells also had improved mitochondrial function, less cytoplasmic chromatin aw well as produced less inflammatory signals. Similar beneficial effects were observed in mice when examining the livers of mice in which senescence was induced through high doses of acetaminophen or radiation. However, the side effects of the inhibitor which include nausea and fatigue may make the drugs too toxic for use in preventing diseases in healthy humans. Next phase in this research is to screen for a less toxic senescence inhibiting drug. 

"This study provides the first concrete link between several known hallmarks of aging -- dysfunctional mitochondria, inflammation and senescent cells -- which historically were studied as separate events," says Adams. "We are hopeful that targeting the molecular drivers of senescence will lead us to safe and effective medicines that help more people stay as healthy as possible, for as long as possible."

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This article is not intended to provide medical diagnosis, advice, treatment, or endorsement.

https://www.sciencedaily.com/releases/2020/02/200220091534.htm

https://www.sbpdiscovery.org/news/a-deep-dive-into-cellular-aging

http://dx.doi.org/10.1101/gad.331272.119

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