{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,27]],"date-time":"2026-05-27T14:09:18Z","timestamp":1779890958273,"version":"3.53.1"},"reference-count":50,"publisher":"SAGE Publications","issue":"7","license":[{"start":{"date-parts":[[2026,4,23]],"date-time":"2026-04-23T00:00:00Z","timestamp":1776902400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["DNA and Cell Biology"],"published-print":{"date-parts":[[2026,7,1]]},"abstract":"<jats:p>\n                    This study aims to investigate the expression of the SLC25 subfamily in sepsis-associated acute kidney injury (SA-AKI) and the role of\n                    <jats:italic toggle=\"yes\">SLC25A30<\/jats:italic>\n                    in regulating PINK1\/PARKIN-mediated mitophagy. Transcriptome sequencing of renal tissues from lipopolysaccharide (LPS)-induced SA-AKI rats at multiple time points revealed time-dependent differential expression of SLC25 genes. At 12 h post-LPS injection (renal injury peak), 11 differentially expressed genes were identified. Intersection with Gene Expression Omnibus datasets and Gene Ontology enrichment highlighted 11 codifferentially expressed genes enriched in mitochondrial transmembrane transport. Notably,\n                    <jats:italic toggle=\"yes\">SLC25A30<\/jats:italic>\n                    was significantly negatively correlated with KIM-1 (\n                    <jats:italic toggle=\"yes\">r<\/jats:italic>\n                    = \u20130.96) and LCN2 (\n                    <jats:italic toggle=\"yes\">r<\/jats:italic>\n                    = \u20130.98).\n                    <jats:italic toggle=\"yes\">SLC25A30<\/jats:italic>\n                    was significantly downregulated in SA-AKI rat renal tissues and LPS-induced HK-2 cells, accompanied by upregulated PINK1\/PARKIN, excessive mitophagy (elevated LC3B-II, decreased p62), and increased renal injury markers.\n                    <jats:italic toggle=\"yes\">SLC25A30<\/jats:italic>\n                    overexpression inhibited PINK1\/PARKIN, reversed excessive mitophagy, reduced KIM-1 and LCN2 levels, alleviated mitochondrial dysfunction, enhanced cell viability, and exerted cytoprotective effects.\n                    <jats:italic toggle=\"yes\">PINK1<\/jats:italic>\n                    knockdown attenuated the regulatory effect of\n                    <jats:italic toggle=\"yes\">SLC25A30<\/jats:italic>\n                    on excessive mitophagy, indicating a dependence on the PINK1\/PARKIN pathway. In conclusion, downregulated\n                    <jats:italic toggle=\"yes\">SLC25A30<\/jats:italic>\n                    is closely associated with excessive mitophagy in SA-AKI.\n                    <jats:italic toggle=\"yes\">SLC25A30<\/jats:italic>\n                    overexpression inhibits excessive mitophagy via downregulating the PINK1\/PARKIN pathway, improves mitochondrial function, and alleviates HK-2 cell injury, suggesting that\n                    <jats:italic toggle=\"yes\">SLC25A30<\/jats:italic>\n                    may be a novel molecular target for SA-AKI-targeted therapy.\n                  <\/jats:p>","DOI":"10.1177\/10445498261442835","type":"journal-article","created":{"date-parts":[[2026,4,24]],"date-time":"2026-04-24T06:39:13Z","timestamp":1777012753000},"page":"327-342","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["SLC25A30 Regulates Mitochondrial Autophagy Through the PINK1\/PARKIN Signaling Pathway to Alleviate Sepsis-Associated Acute Kidney Injury"],"prefix":"10.1177","volume":"45","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-0429-9705","authenticated-orcid":false,"given":"Mingyu","family":"Xu","sequence":"first","affiliation":[{"name":"Department of Clinical Laboratory, The First Affiliated Hospital of Harbin Medical University, Harbin, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuchen","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Blood Transfusion, Xi\u2019an People\u2019s Hospital (Xi\u2019an fourth hospital), Affiliated People\u2019s Hospital of Northwest University, Xi\u2019an, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wuyang","family":"Lv","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory, Shangluo Central Hospital, Shangluo, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yingyue","family":"Ding","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory, The First Affiliated Hospital of Harbin Medical University, Harbin, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory, The First Affiliated Hospital of Harbin Medical University, Harbin, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruxue","family":"Diao","sequence":"additional","affiliation":[{"name":"Department of Blood Transfusion, The First Affiliated Hospital of Medical College of Zhejiang University, Hangzhou, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaotong","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory, The First Affiliated Hospital of Harbin Medical University, Harbin, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mengjiao","family":"Yin","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory, The First Affiliated Hospital of Harbin Medical University, Harbin, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yingyu","family":"Jin","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory, The First Affiliated Hospital of Harbin Medical University, Harbin, 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