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In aged EOC\u2010bearing mice, we observed reduced survival, accompanied by impaired CD4\n                    <jats:sup>+<\/jats:sup>\n                    and CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cell responses and a marked expansion of FOXP3\n                    <jats:sup>+<\/jats:sup>\n                    Tregs exhibiting elevated IL\u201010 and TGF\u03b2 expression. Metabolic profiling revealed enhanced oxidative phosphorylation in Tregs from aged mice, along with a fivefold increase in intracellular succinate levels. This accumulation of succinate within the aged tumor microenvironment was found to potentiate Treg suppressive function. Notably, pharmacologic inhibition of \u03b1\u2010ketoglutarate dehydrogenase reversed this effect, restoring effector T cell activity. These findings highlight succinate\u2010driven metabolic reprogramming as a central mechanism of age\u2010related Treg dysfunction in EOC and suggest that targeting succinate metabolism may offer a promising strategy to rejuvenate antitumor immunity in elderly patients.\n                  <\/jats:p>","DOI":"10.1111\/acel.70510","type":"journal-article","created":{"date-parts":[[2026,4,25]],"date-time":"2026-04-25T06:54:21Z","timestamp":1777100061000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Aging\u2010Driven Immunosuppression: The Role of Tregs in the Ovarian Tumor Microenvironment"],"prefix":"10.1111","volume":"25","author":[{"given":"Mary P.","family":"Udumula","sequence":"first","affiliation":[{"name":"Division of Gynecologic Oncology Henry Ford Hospital  Detroit Michigan USA"},{"name":"Henry Ford Cancer Institute  Detroit Michigan USA"},{"name":"Department of Obstetrics, Gynecology &amp; Reproductive 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