ArticleCell communication and signaling : CCS2025
REST contributes to renal fibrosis through inducing mitochondrial energy metabolism imbalance in tubular epithelial cells.
Article in Cell communication and signaling : CCS, 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.
- An Emerging Role for OGDHL: From Mitochondrial Energy Metabolism to Neurodevelopmental Disorders.Biology · 2025Review
- Unraveling the mysteries of the gut-kidney axis: the protective role of traditional Chinese medicine in chronic kidney disease.Frontiers in microbiology · 2025Review
- Solute carrier family 1 member 1 in renal interstitial fibrosis: evaluating its influence on glutamate uptake and extracellular ion levels.Frontiers in medicine · 2025Article
- Vericiguat attenuates cyclosporine A-induced nephropathy by targeting the NF-κB/TGF-β1 axis: an integrated network pharmacology, Mendelian randomization, and experimental study.Frontiers in immunology · 2025Article
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Abstract
backgroundRenal fibrosis represents the final common pathological manifestation of chronic kidney disease (CKD), yet the underlying mechanism remains elusive, and there is still a lack of effective targeted therapeutic strategy. Although previous research indicated that repressor element 1-silencing transcription factor (REST) contributed to acute kidney injury (AKI) in renal tubular epithelial cells (RTECs), its specific contribution to renal fibrosis and associated mechanisms remains largely unexplored.
methodsRenal biopsies from CKD patients were collected to evaluate the expression of REST. Kidney-specific Rest conditional knockout (Cdh16-Cre/Rest
resultsREST was significantly up-regulated in the kidney tissues from CKD patients, UUO-induced fibrotic mouse models and TGF-β1-incubated RTECs. Notably, kidney-specific knockout of Rest prominently alleviated renal fibrosis by improving mitochondrial energy metabolism and restoring fatty acid oxidation. Mechanically, REST disturbed mitochondrial energy metabolism through repressing the transcription of oxoglutarate dehydrogenase-like (OGDHL) via directly binding to its promotor region. Further, pharmacological inhibition of REST using the specific REST inhibitor, X5050, significantly ameliorated the progression of renal fibrosis both in vitro and in vivo.
conclusionsOur explorations revealed the upregulation of REST in renal fibrosis disrupts mitochondrial energy metabolism through transcriptionally suppressing OGDHL, which may act as a promising therapeutic target for renal fibrosis.
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