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The biological logic is that telomere shortening in dermal fibroblasts occurring over decades of UV exposure, oxidative stress, and replication is a primary driver of fibroblast functional decline and senescence-driven dermal thinning

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However, recent work has shown that, in addition to using histones as substrates for deacetylation, HDACs can also inhibit the acetylation of non-histone proteins and modulate diverse neurobiological processes [59, 60]