ArticleRenal failure2025
Arfgef3 knockout ameliorates ischemia reperfusion-induced acute kidney injury via mitochondrial dysfunction alleviation in mice.
Article in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Ischemia reperfusion-induced acute kidney injury (IRI-AKI) is a prevalent clinical complication among hospitalized patients with high morbidity and mortality. Mitochondria, as crucial organelles for maintaining cellular homeostasis, play a pivotal role in IRI-AKI pathogenesis. Currently, no effective and definitive therapeutic targets have been established for IRI-AKI treatment. Previous sequencing data analysis revealed significant upregulation of Arfgef3 following renal ischemia-reperfusion injury, suggesting its potential as a therapeutic target. This study demonstrates that Arfgef3 expression is markedly elevated after ischemia reperfusion injury. Furthermore, Arfgef3 knockout (KO) significantly ameliorated renal injury induced by ischemia-reperfusion in mice. In addition, Arfgef3 knockout effectively attenuates renal inflammation (IL6, MCP1, TNF-α), oxidative stress and apoptosis levels. In addition, Arfgef3 knockout substantially improves ischemia reperfusion-induced mitochondrial abnormalities including mitochondrial biogenesis markers and ATP production capacity. In conclusion, Arfgef3 participates in IRI-AKI pathogenesis by regulating mitochondrial function. Arfgef3 knockout confers renal protection through improving mitochondrial dysfunction, thereby reducing inflammatory response, oxidative stress and apoptosis. These findings provide novel insights into IRI-AKI mechanisms and highlight Arfgef3 as a potential therapeutic target.
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