{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T06:01:02Z","timestamp":1784700062140,"version":"3.55.0"},"reference-count":36,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T00:00:00Z","timestamp":1783382400000},"content-version":"vor","delay-in-days":6,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100007129","name":"Natural Science Foundation of Shandong Province","doi-asserted-by":"publisher","award":["ZR2025MS1227"],"award-info":[{"award-number":["ZR2025MS1227"]}],"id":[{"id":"10.13039\/501100007129","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82470722"],"award-info":[{"award-number":["82470722"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82270724"],"award-info":[{"award-number":["82270724"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81970582"],"award-info":[{"award-number":["81970582"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81800601"],"award-info":[{"award-number":["81800601"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100019558","name":"Qingdao Key Health Discipline Development Fund","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100019558","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Nephrology"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>To explore the regulation and function of serum response factor (SRF)\/Cellular communication network factor 1 (CCN1) pathway in ferroptosis in ischemia\/reperfusion (I\/R) acute kidney injury (AKI).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>The level of SRF, CCN1, ferroptosis markers (TFR1, ACSL4, xCT, GPX4), ROS and SOD were examined in HK\u20102 cells under hypoxia\/reoxygenation (H\/R) treatment or rat renal tissue samples after I\/R treatment. SRF was overexpressed by pcDNA\u2010SRF plasmid and suppressed by CCG\u20101423 (a small molecule inhibitor of SRF) or SRF siRNA to study how SRF influences ferroptosis through CCN1 in I\/R AKI.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In HK\u20102 cells under H\/R treatment and renal tissue from I\/R rats, the SRF along with CCN1, TFR1 and ACSL4 expression was upregulated, while xCT and GPX4 expression was downregulated. SRF upregulation in HK\u20102 cells increased CCN1 expression and was associated with ferroptosis\u2010related changes. Blockade of SRF by CCG\u20101423 or an SRF\u2010specific siRNA reduced CCN1 induction, protected renal tubular epithelial cells from ferroptosis\u2010related injury, and alleviated I\/R AKI both in\u00a0vitro and in\u00a0vivo.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Increased SRF\/CCN1 pathway activity may be associated with ferroptosis\u2010related injury and dysfunction in renal tubular epithelial cells during AKI. Targeting SRF with CCG\u20101423 may represent a potential therapeutic strategy of AKI.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/nep.70244","type":"journal-article","created":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T00:04:26Z","timestamp":1783469066000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Serum Response Factor Regulates\n                    <scp>CCN1<\/scp>\n                    to Exacerbate Acute Kidney Injury Through Facilitation of Ferroptosis\u2010Related Injury"],"prefix":"10.1111","volume":"31","author":[{"given":"Yanfei","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Nephrology The Affiliated Hospital of Qingdao University  Qingdao China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chen","family":"Guan","sequence":"additional","affiliation":[{"name":"Department of Nephrology The Affiliated Hospital of Qingdao University  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