One of the most fundamental questions in biology is how we age. The past decades have witnessed a significant revision of a traditional view that aging is simply a random and passive process that is solely driven by entropy. In fact, the aging process is regulated genetically and lifespan can be extended by single gene mutations. The Chen Lab research aims to understand molecular and cellular mechanisms that regulate the aging process and explore therapeutic targets to slow aging and even reverse aging-associated degeneration. The most intriguing aspect of pharmaceutical intervention that targets the aging pathways is that, instead of targeting a specific disease, it has the potential of ameliorating a wide array of seemingly unrelated diseases associated with aging, such as cancer, tissue degeneration, metabolic syndrome, and immune dysfunction.
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UC Berkeley scientists have identified a new molecular pathway critical to aging. They found that by slowing down the activity of mitochondria in the blood stem cells of mice, they could enhance the cells’ capacity to handle stress and rejuvenate old blood.
A new study led by researchers at the University of California, Berkeley, represents a major advance in the understanding of the molecular mechanisms behind aging while providing new hope for the development of targeted treatments for age-related degenerative diseases.