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Through unbiased global metabolomic profiling of peri\u2010implantation uteri across different ages in mice, we identified nicotinamide adenine dinucleotide (NAD\n                    <jats:sup>+<\/jats:sup>\n                    ) depletion as a hallmark metabolic feature of endometrial aging. Single\u2010cell RNA sequencing further revealed an expansion of senescent stromal cell populations, which was accompanied by a decline in NAD\n                    <jats:sup>+<\/jats:sup>\n                    levels. Supplementation with NAD\n                    <jats:sup>+<\/jats:sup>\n                    precursors alleviated age\u2010related stromal senescence and endometrial dysfunction, thereby restoring the uterus' implantation competence. Mechanically, we demonstrate that CD38 derived from myeloid serves as a principal driver of uterine NAD\n                    <jats:sup>+<\/jats:sup>\n                    depletion; this process accelerates stromal senescence and impairs uterine receptivity. These findings establish CD38 as a central physiological integrator that links NAD\n                    <jats:sup>+<\/jats:sup>\n                    metabolism to uterine function and highlight it as a promising target for rejuvenation strategies aimed at improving reproductive outcomes in women of advanced maternal age.\n                  <\/jats:p>","DOI":"10.1111\/acel.70356","type":"journal-article","created":{"date-parts":[[2025,12,29]],"date-time":"2025-12-29T05:50:49Z","timestamp":1766987449000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Myeloid\u2010Derived\n                    <scp>CD38<\/scp>\n                    Mediates Age\u2010Related Endometrial Aging Through\n                    <scp>NAD<\/scp>\n                    <sup>+<\/sup>\n                    Depletion"],"prefix":"10.1111","volume":"25","author":[{"given":"Lun","family":"Hua","sequence":"first","affiliation":[{"name":"Animal Nutrition 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