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Using serum proteomics, we identified the senescence-associated secretory phenotype (SASP), a marker of cellular senescence associated with biological aging, as the most highly up-regulated pathway in young women with PPCM or preeclampsia. Placentas from women with preeclampsia displayed multiple markers of amplified senescence and tissue aging, as well as overall increased gene expression of 28 circulating proteins that contributed to SASP pathway enrichment in serum samples from patients with preeclampsia or PPCM. The most highly expressed placental SASP factor, activin A, was associated with cardiac dysfunction or heart failure severity in women with preeclampsia or PPCM. In a murine model of PPCM induced by cardiomyocyte-specific deletion of the gene encoding peroxisome proliferator\u2013activated receptor \u03b3 coactivator-1\u03b1, inhibiting activin A signaling in the early postpartum period with a monoclonal antibody to the activin type II receptor improved heart function. In addition, attenuating placental senescence with the senolytic compound fisetin in late pregnancy improved cardiac function in these animals. These findings link senescence biology to cardiac dysfunction in pregnancy and help to elucidate the pathogenesis underlying cardiovascular diseases of pregnancy.<\/jats:p>","DOI":"10.1126\/scitranslmed.adi0077","type":"journal-article","created":{"date-parts":[[2024,4,17]],"date-time":"2024-04-17T13:58:38Z","timestamp":1713362318000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":44,"title":["Placental senescence pathophysiology is shared between peripartum cardiomyopathy and preeclampsia in mouse and human"],"prefix":"10.1126","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6999-6868","authenticated-orcid":true,"given":"Jason D.","family":"Roh","sequence":"first","affiliation":[{"name":"Corrigan Minehan Heart Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, 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