{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T02:52:39Z","timestamp":1772074359138,"version":"3.50.1"},"reference-count":0,"publisher":"S. Karger AG","issue":"4","license":[{"start":{"date-parts":[[2023,11,13]],"date-time":"2023-11-13T00:00:00Z","timestamp":1699833600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/karger.com\/pages\/terms-and-conditions"},{"start":{"date-parts":[[2023,11,13]],"date-time":"2023-11-13T00:00:00Z","timestamp":1699833600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/karger.com\/pages\/terms-and-conditions"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nephron"],"published-print":{"date-parts":[[2024]]},"abstract":"<jats:p>&lt;b&gt;&lt;i&gt;Introduction:&lt;\/i&gt;&lt;\/b&gt; Suppressor of cytokine signaling 3 (SOCS3) is highly expressed in mice with renal ischemia\/reperfusion (RI\/R) injury and has the potential to regulate mitophagy. On this basis, this study further investigates the possible mechanism via which SOCS3 affects RI\/R by regulating mitophagy. &lt;b&gt;&lt;i&gt;Method:&lt;\/i&gt;&lt;\/b&gt; After establishing a RI\/R injury mouse model and a hypoxia\/reoxygenation (H\/R) cell model, the effects of silenced SOCS3 on injury and mitophagy in the above models were analyzed by ELISA, quantitative real-time polymerase chain reaction, Western blot, pathological sections, CCK-8 assay, flow cytometry, and JC-1 assay. Mechanistic studies were carried out with the help of database analysis and binding validation experiments (chromatin immunoprecipitation, dual-luciferase reporter assay, and co-immunoprecipitation). After the binding target was identified, the regulatory relationship between the target gene and SOCS3 was verified by rescue experiments. &lt;b&gt;&lt;i&gt;Result:&lt;\/i&gt;&lt;\/b&gt; The large increase in blood urea nitrogen (BUN) and creatinine (Cr) levels verified the success of the RI\/R model. SOCS3 expression was up-regulated in RI\/R mice. Silenced SOCS3 alleviated kidney damage and mitochondrial abnormalities in RI\/R mice and inhibited mitophagy at the molecular level. Likewise, silenced SOCS3 alleviated H\/R-induced cell damage and mitophagy. Finally, activating transcription factor 3 (ATF3) was determined to bind to the promoter of SOCS3, which interacted with insulin-like growth factor 1 receptor (IGF1R). Rescue experiments confirmed the effect of ATF3 on SOCS3 expression and the underlying regulatory mechanism. &lt;b&gt;&lt;i&gt;Conclusion:&lt;\/i&gt;&lt;\/b&gt; ATF3 mediates SOCS3 expression to promote the activation of mitophagy, thereby aggravating renal ischemia-reperfusion injury. <\/jats:p>","DOI":"10.1159\/000531912","type":"journal-article","created":{"date-parts":[[2023,11,13]],"date-time":"2023-11-13T22:00:38Z","timestamp":1699912838000},"page":"230-244","source":"Crossref","is-referenced-by-count":4,"title":["Transcription Factor ATF3 Mediating SOCS3 Expression Aggravates Renal Ischemia-Reperfusion Injury by Activating Mitophagy"],"prefix":"10.1159","volume":"148","author":[{"given":"Yu","family":"Luo","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhitao","family":"Cai","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiongfei","family":"Wu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Feng","family":"Liu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lian","family":"Li","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"127","published-online":{"date-parts":[[2023,11,13]]},"container-title":["Nephron"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/karger.com\/nef\/article-pdf\/148\/4\/230\/4187211\/000531912.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/karger.com\/nef\/article-pdf\/148\/4\/230\/4187211\/000531912.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T15:40:25Z","timestamp":1745422825000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000531912"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2023,11,13]]},"references-count":0,"journal-issue":{"issue":"4","published-online":{"date-parts":[[2024,4,2]]},"published-print":{"date-parts":[[2024,3,28]]}},"URL":"https:\/\/doi.org\/10.1159\/000531912","archive":["Portico"],"relation":{"is-supplemented-by":[{"id-type":"doi","id":"10.6084\/m9.figshare.24550744","asserted-by":"subject"}]},"ISSN":["1660-8151","2235-3186"],"issn-type":[{"value":"1660-8151","type":"print"},{"value":"2235-3186","type":"electronic"}],"subject":[],"published":{"date-parts":[[2023,11,13]]}}}