Destroying inflammatory ‘zombie’ cells could slow age-related disease

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For decades, scientists had ignored senescent cells—which are trapped in a long-term state of cell cycle arrest—dismissing them as artifacts of cell culture with no significance inside living organisms. But in recent years, [researcher James] Kirkland and other researchers have established senescence as an important physiological process that appears to play seemingly opposing roles in vivo. On the one hand, senescent cells are thought to mediate tissue development when they form in the embryo, and also to promote tissue regeneration and wound repair in later life. However, as these zombie cells accumulate with age, they can ooze inflammatory proteins believed to cause tissue dysfunction and to push neighboring cells into senescence.

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Kirkland and others have cautiously launched a wave of clinical studies to evaluate whether senolytic agents offer promise in treating serious age-related ailments such as osteoarthritis, kidney and lung fibrosis, and Alzheimer’s disease. Although many questions remain about senescence and its role in the aging process, these researchers argue that unlike other agents hyped as elixirs of youth that have repeatedly failed to show benefits in clinical studies, the concept of senolytics will stand the test of time.

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