{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T10:45:13Z","timestamp":1792147513424,"version":"4.4.0"},"reference-count":40,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T00:00:00Z","timestamp":1791763200000},"content-version":"vor","delay-in-days":11,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:00:00Z","timestamp":1790812800000},"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":["82460424"],"award-info":[{"award-number":["82460424"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cell Biology International"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Legg\u2010Calv\u00e9\u2010Perthes disease (LCPD) causes malformations of femoral head in children, which presents as a treatment challenge due to its unclear pathogenesis. This study aimed to investigate the influence of circCDR1as on LCPD and its related mechanisms. An in vivo LCPD model was established in spontaneously hypertensive rats (SHRs) and HMGB1\u2010stimulated chondrocytes were used to mimic LCPD in vitro. We found that circCDR1as was up\u2010regulated, while miR\u2010671\u20105p was down\u2010regulated in LCPD patients, which exhibited a negative correlation. Depletion of circCDR1as restored the proliferation and inhibited \u2010ferroptosis of HMGB1\u2010exposed chondrocytes, Mechanistically, circCDR1as silencing increased miR\u2010671\u20105p expression that targeted NCOA4 mRNA to disrupt the NCOA4\u2010FTH1 interaction\u2010mediated ferritinophagy. Moreover, treatment with conditioned medium (CM) of circCDR1as\u2010silenced chondrocytes repressed M1 macrophage polarization via enhancing miR\u2010671\u20105p expression that subsequently targeted TLR4 mRNA to inactivate TLR4\/NF\u2010\u03baB pathway. FUS was responsible for circCDR1as biogenesis via the direct binding to pre\u2010CDR1as mRNA. Collectively, chondrocyte ferroptosis was triggered by FUS\u2010activated circCDR1as via sponging miR\u2010671\u20105p to enhance NCOA4\u2010FTH1 interaction\u2010mediated ferritinophagy, which resulted in M1 macrophage reprogramming via activating the TLR4\/NF\u2010\u03baB pathway, thus promoting LCPD development.<\/jats:p>","DOI":"10.1002\/cbin.70207","type":"journal-article","created":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T13:43:20Z","timestamp":1791812600000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["circCDR1as\/miR\u2010671\u20105p Axis Modulates Chondrocyte Ferroptosis and Macrophage Reprogramming via Targeting NCOA4 and TLR4 in Legg\u2010Calv\u00e9\u2010Perthes Disease"],"prefix":"10.1002","volume":"50","author":[{"given":"Quan","family":"Liu","sequence":"first","affiliation":[{"name":"Orthopedic Hospital, The First Affiliated Hospital, Jiangxi Medical College Nanchang University Nanchang 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