{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T15:19:45Z","timestamp":1787757585329,"version":"build-2784847793"},"reference-count":33,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2026,8,2]],"date-time":"2026-08-02T00:00:00Z","timestamp":1785628800000},"content-version":"vor","delay-in-days":1,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,8,1]],"date-time":"2026-08-01T00:00:00Z","timestamp":1785542400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82471690"],"award-info":[{"award-number":["82471690"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004826","name":"Natural Science Foundation of Beijing Municipality","doi-asserted-by":"publisher","award":["7242003"],"award-info":[{"award-number":["7242003"]}],"id":[{"id":"10.13039\/501100004826","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Molecular Reproduction Devel"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Post\u2010ovulatory aging (POA) reduces oocyte quality, yet effective interventions remain limited. Here we demonstrate that early intervention with vitamin K2 (menaquinone\u20104 isoform, MK\u20104) alleviates POA by inhibiting iron\u2010disorder\u2010induced oxidative stress. Western blot revealed that the expressions of ferroptosis suppressor protein 1 (FSP1) and vitamin K epoxide reductase\u2010like protein (VKORC1L1) were significantly decreased in mouse POA oocytes; however, MK\u20104 attenuated these changes. Further, MK\u20104 inhibited ferritinophagy by downregulating NCOA4 and LC3II, markedly restored ferritin level, reduced intracellular Fe\n                    <jats:sup>2+<\/jats:sup>\n                    amount, thus attenuating oxidative stress. These results were characterized by reducing lipid peroxidation marker malondialdehyde (MDA) and acyl\u2010CoA synthetase long chain family member 4 (ACSL4) expression, decreasing \u03b3\u2010H2AX and 8\u2010Hydroxy\u20102\u2032\u2010deoxyguanosine (8\u2010OHdG), and enhancing expression of the mitochondrial antioxidant enzyme superoxide dismutase 1 (SOD1). Additionally, MK\u20104 suppressed mitophagy by downregulating PINK1 and Parkin, and upregulating Rab7 improving mitochondrial membrane potential. Consequently, abnormalities in chromosomes, spindles, and the cytoskeleton were significantly ameliorated in POA oocytes receiving early MK\u20104 intervention. Notably, in vitro\u2010aging oocytes expressed higher FSP1 and VKORC1L1 but lower ACSL4 and MDA versus the in vivo counterparts, suggesting a milder lipid peroxidation in vitro. Collectively, our findings uncover a novel anti\u2010aging mechanism triggered by MK\u20104, highlighting its potential to establish a preventive strategy for female reproductive aging.\n                  <\/jats:p>","DOI":"10.1002\/mrd.70141","type":"journal-article","created":{"date-parts":[[2026,8,2]],"date-time":"2026-08-02T16:55:37Z","timestamp":1785689737000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["MK\u20104 Ameliorates Post\u2010Ovulatory Aging of Mouse Oocytes by Alleviating Iron Metabolism Disorder\u2010Induced Oxidative Stress"],"prefix":"10.1002","volume":"93","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-3346-1059","authenticated-orcid":false,"given":"Yangzi","family":"Zheng","sequence":"first","affiliation":[{"name":"Department of Histology and Embryology, School of Basic Medical Sciences Capital Medical University Beijing China"},{"name":"Fuwai Hospital Chinese Academy of Medical Sciences 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