ArticleCell biology and toxicology2026
HucMSC-EVs attenuate renal fibrosis via miR-874-3p-mediated inhibition of cGAS-STING signaling.
Article in Cell biology and toxicology, 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
Chronic kidney disease (CKD) is characterized by progressive renal interstitial fibrosis, which is closely associated with tubular epithelial cell injury, mitochondrial dysfunction, and aberrant inflammatory signaling. Our previous studies demonstrated that extracellular vesicles derived from human umbilical cord mesenchymal stem cells (HucMSC-EVs) effectively alleviate renal fibrosis in a unilateral ureteral obstruction (UUO) model. Based on these findings, the present study further investigated the molecular mechanisms underlying the anti-fibrotic effects of HucMSC-EVs. Using a cisplatin-induced HK-2 cell injury model, we evaluated the effects of HucMSC-EVs on epithelial-mesenchymal transition (EMT) and fibrosis. The results showed that HucMSC-EVs attenuated EMT and fibrotic phenotypes in vitro. Consistently, in UUO-induced kidneys, HucMSC-EVs improved renal histopathological injury and alleviated fibrosis. Mechanistically, HucMSC-EVs reduced mitochondrial reactive oxygen species (mtROS) levels and inhibited abnormal opening of the mitochondrial permeability transition pore (mPTP), thereby preserving mitochondrial homeostasis and suppressing activation of the cGAS-STING signaling pathway. The involvement of this pathway was further confirmed using the STING inhibitor C-176. In addition, we validated that miR-874-3p contributes to these protective effects, as its overexpression partially recapitulated the function of HucMSC-EVs. Collectively, these findings suggest that HucMSC-EVs attenuate renal fibrosis by modulating mitochondrial function and inhibiting the cGAS-STING pathway, providing mechanistic insight into EV-mediated protection in kidney injury.
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