ArticleTranslational andrology and urology2026
Overexpression of SIRT3 ameliorates calcium oxalate crystal-induced renal necroptosis by suppressing the TNF-α/RIPK3/P-MLKL pathway.
Article in Translational andrology and urology, 2026. 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
Background: The molecular mechanisms by which SIRT3 regulates calcium oxalate (CaOx) crystal-induced necroptosis in renal tubular epithelial cells and attenuates crystal formation and adhesion remain unclear. This study aims to investigate these underlying mechanisms. Methods: A mouse model of renal (Male C57BL/6J mice) CaOx crystal deposition was established by intraperitoneal glyoxylate injection, and HK-2 cells were treated with CaOx crystals. SIRT3 expression was genetically modulated, and Necrostatin-1 (a TNF-α inhibitor) was administered. The following evaluations were performed: cell viability assay, malondialdehyde (MDA) level detection, renal crystal deposition assessment by von Kossa staining, renal tissue injury evaluation by hematoxylin and eosin staining, and the expression levels of RIPK1, RIPK3, MLKL, p-MLKL, and TNF-α detected via Western blot and immunohistochemistry. Results: SIRT3 overexpression significantly ameliorated CaOx-induced renal necroptosis, tissue damage, and crystal deposition in mice. In HK-2 cells, SIRT3 overexpression promoted cell recovery, reduced CaOx-induced cytotoxicity, and suppressed MDA production. Additionally, CaOx stimulation strongly activated TNF-α signaling in HK-2 cells, while Necrostatin-1 mitigated necroptosis. Moreover, SIRT3 was found to be downregulated in CaOx-stimulated renal tissues. Conclusions: Overexpression of SIRT3 attenuates CaOx-induced necroptosis in renal tubular epithelial cells and reduces renal crystal deposition in mice, which is likely mediated through the suppression of the TNF-α/RIPK1/RIPK3/p-MLKL pathway.
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