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We previously found genetic clearance of senescent cells from progeroid INK-ATTAC mice prevents lipodystrophy. Here we show that primary human senescent fat progenitors secrete activin A and directly inhibit adipogenesis in non-senescent progenitors. Blocking activin A partially restored lipid accumulation and expression of key adipogenic markers in differentiating progenitors exposed to senescent cells. Mouse fat tissue activin A increased with aging. Clearing senescent cells from 18-month-old naturally-aged INK-ATTAC mice reduced circulating activin A, blunted fat loss, and enhanced adipogenic transcription factor expression within 3 weeks. JAK inhibitor suppressed senescent cell activin A production and blunted senescent cell-mediated inhibition of adipogenesis. Eight weeks-treatment with ruxolitinib, an FDA-approved JAK1\/2 inhibitor, reduced circulating activin A, preserved fat mass, reduced lipotoxicity, and increased insulin sensitivity in 22-month-old mice. Our study indicates targeting senescent cells or their products may alleviate age-related dysfunction of progenitors, adipose tissue, and metabolism.<\/jats:p>","DOI":"10.7554\/elife.12997","type":"journal-article","created":{"date-parts":[[2015,12,19]],"date-time":"2015-12-19T07:32:53Z","timestamp":1450510373000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.12997","source":"Crossref","is-referenced-by-count":576,"title":["Targeting senescent cells enhances adipogenesis and metabolic function in old age"],"prefix":"10.7554","volume":"4","author":[{"given":"Ming","family":"Xu","sequence":"first","affiliation":[{"name":"Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allyson K","family":"Palmer","sequence":"additional","affiliation":[{"name":"Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, United 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