ArticleScientific reports2026
Downregulation of CXCL16/ADAM10 axis by Simvastatin attenuates tacrolimus-induced tubulointerstitial fibrosis.
Article in Scientific reports, 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
Tacrolimus (TAC), a widely used immunosuppressive agent, is associated with significant nephrotoxicity characterized by renal inflammation and fibrosis. Simvastatin (SIM), beyond its lipid-lowering effects, exhibits pleiotropic anti-inflammatory and anti-fibrotic properties. This study aimed to explore the protective effect of SIM against TAC-induced renal injury, with a focus on the potential involvement of the CXCL16/ADAM10 signaling axis. Adult male Wistar rats were divided into four groups (n = 10 per group): control, SIM-treated (SIM; 10 mg/kg/day), TAC-treated (TAC; 2 mg/kg/day), and SIM + TAC-treated. All medications were given orally for 28 days. Hematological indices, renal function parameters, and lipid profile were assessed. Histopathological evaluation and immunofluorescence analysis of CXCL16, ADAM10, fibronectin and TGF-β were performed. TAC administration resulted in significant renal dysfunction, dyslipidemia, and marked histopathological alterations, accompanied by upregulation of CXCL16, ADAM10, and fibrotic markers. Conversely, co-administration of SIM and TAC improved renal function, attenuated lipid abnormalities, and preserved renal architecture. These effects were associated with decreased the expression of CXCL16, ADAM10, TGF-β and fibronectin. SIM demonstrates significant kidney-protective properties against TAC-induced renal injury, potentially involving modulation of the CXCL16/ADAM10 signaling pathway. These findings indicate that SIM could be a beneficial supplementary treatment to alleviate the serious kidney-damaging effects associated with TAC.
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