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Unfortunately, there is no report to elucidate the detailed influence of mitochondrial fusion in renal IR injury. This study principally investigated the mechanism by which mitochondrial fusion protected kidney against IR injury. Our results indicated that sirtuin 3 (Sirt3) was inhibited after renal IR injury in vivo and in vitro. Overexpression of Sirt3 improved kidney function, modulated oxidative injury, repressed inflammatory damage, and reduced tubular epithelial cell apoptosis. The molecular investigation found that Sirt3 overexpression attenuated IR\u2010induced mitochondrial damage in renal tubular epithelial cells, as evidenced by decreased reactive oxygen species production, increased antioxidants sustained mitochondrial membrane potential, and inactivated mitochondria\u2010initiated death signaling. In addition, our information also illuminated that Sirt3 maintained mitochondrial homeostasis against IR injury by enhancing optic atrophy 1 (OPA1)\u2010triggered fusion of mitochondrion. Inhibition of OPA1\u2010induced fusion repressed Sirt3 overexpression\u2010induced kidney protection, leading to mitochondrial dysfunction. Further, our study illustrated that OPA1\u2010induced fusion could be affected through ERK; inhibition of ERK abolished the regulatory impacts of Sirt3 on OPA1 expression and mitochondrial fusion, leading to mitochondrial damage and tubular epithelial cell apoptosis. Altogether, our results suggest that renal IR injury is closely associated with Sirt3 downregulation and mitochondrial fusion inhibition. Regaining Sirt3 and\/or activating mitochondrial fission by modifying the ERK\u2010OPA1 cascade may represent new therapeutic modalities for renal IR injury.<\/jats:p>","DOI":"10.1002\/jcp.28918","type":"journal-article","created":{"date-parts":[[2019,6,7]],"date-time":"2019-06-07T12:35:05Z","timestamp":1559910905000},"page":"23495-23506","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":89,"title":["Sirt3 modulate renal ischemia\u2010reperfusion injury through enhancing mitochondrial fusion and activating the ERK\u2010OPA1 signaling pathway"],"prefix":"10.1002","volume":"234","author":[{"given":"Qiang","family":"Wang","sequence":"first","affiliation":[{"name":"Urology Department, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine Tsinghua University Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Junnan","family":"Xu","sequence":"additional","affiliation":[{"name":"Beijing Key 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