ArticleCell biology and toxicology2025
UHRF1 promotes calcium oxalate-induced renal fibrosis by renal lipid deposition via bridging AMPK dephosphorylation.
Article in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- SIRT5-Mediated Desuccinylation of ACAA2 Protects Against Calcium Oxalate-Induced Kidney Injury by Regulating Fatty Acid Oxidation to Suppress Mitochondrial Oxidative Injury and Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- ND-630, an acetyl-CoA carboxylase inhibitor, prevents renal fibrosis in adenine-induced CKD mice.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- ABCA8-positive lipid-metabolic CAFs mediate immunotherapy resistance in TNBC.Frontiers in oncology · 2025Article
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10 authors.
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Abstract
backgroundNephrolithiasis, a common urinary system disorder, exhibits high morbidity and recurrence rates, correlating with renal dysfunction and the increased risk of chronic kidney disease. Nonetheless, the precise role of disrupted cellular metabolism in renal injury induced by calcium oxalate (CaOx) crystal deposition is unclear. The purpose of this study is to investigate the involvement of the ubiquitin-like protein containing PHD and RING finger structural domain 1 (UHRF1) in CaOx-induced renal fibrosis and its impacts on cellular lipid metabolism.
methodsVarious approaches, including snRNA-seq, transcriptome RNA-seq, immunohistochemistry, and western blot analyses, were employed to assess UHRF1 expression in kidneys of nephrolithiasis patients, hyperoxaluric mice, and CaOx-induced renal tubular epithelial cells. Subsequently, knockdown of UHRF1 in mice and cells corroborated its effect of UHRF1 on fibrosis, ectopic lipid deposition (ELD) and fatty acid oxidation (FAO). Rescue experiments using AICAR, ND-630 and Compound-C were performed in UHRF1-knockdown cells to explore the involvement of the AMPK pathway. Then we confirmed the bridging molecule and its regulatory pathway in vitro. Experimental results were finally confirmed using AICAR and chemically modified si-UHRF1 in vivo of hyperoxaluria mice model.
resultsMechanistically, UHRF1 was found to hinder the activation of the AMPK/ACC1 pathway during CaOx-induced renal fibrosis, which was mitigated by employing AICAR, an AMPK agonist. As a nuclear protein, UHRF1 facilitates nuclear translocation of AMPK and act as a molecular link targeting the protein phosphatase PP2A to dephosphorylate AMPK and inhibit its activity.
conclusionThis study revealed that UHRF1 promotes CaOx -induced renal fibrosis by enhancing lipid accumulation and suppressing FAO via inhibiting the AMPK pathway. These findings underscore the feasible therapeutic implications of targeting UHRF1 to prevent renal fibrosis due to stones.
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