ArticleMolecular therapy : the journal of the American Society of Gene Therapy2025
ATGL regulates renal fibrosis by reprogramming lipid metabolism during the transition from AKI to CKD.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Lactate induces renal lipid accumulation and aggravates renal fibrosis by inhibiting the PPARα signaling pathway and fatty acid oxidation.Renal failure · 2026Article
- The lactate-lactylation axis in acute kidney injury: mechanisms from metabolic reprogramming to epigenetic regulation and clinical therapeutic prospects.International urology and nephrology · 2026Review
- Pharmacological targeting of kidney fibrosis: druggable mechanisms, translational models, and emerging antifibrotic therapies.Clinical kidney journal · 2026Review
- Metabolic reprogramming in fibrosis-related diseases: underlying mechanisms and therapeutics.Molecular biomedicine · 2026Review
- Regulated cell death: a multidimensional regulatory network in the pathogenesis of renal fibrosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Fatty Kidney: The Interplay of Lipids and Diabetic Kidney Disease.Biomedicines · 2026Review
- Inhibiting lactylation for efficient treatment of renal fibrosis through targeting nanomedicine of renal lactate accumulation in obstructed kidney.Journal of nanobiotechnology · 2026Article
- Targeting CH25H/25HC-ferroptosis axis: a novel mechanism of MSC-EVs mediated renoprotection in ischemic AKI.Journal of nanobiotechnology · 2026Article
- Temporal Proteomic and Phosphoproteomic Profiling Deciphers Molecular Dynamics of Acute-to-Chronic Kidney Disease After Ischemia-Reperfusion Injury, With Dock2 Emerging as a Key Regulator.Molecular & cellular proteomics : MCP · 2026Article
- Multi-omics integration identifies Acsm2/ACSM2A deficiency as a metabolic driver of ZBP1-mediated PANoptosis in acute kidney injury.Frontiers in cell and developmental biology · 2026Article
- Lipid metabolism drives podocyte injury in diabetic kidney disease.Frontiers in immunology · 2026Review
- Targeting tubular epithelial cell metabolism to halt renal fibrosis: current evidence and future directions.Frontiers in cell and developmental biology · 2026Review
- Single-cell transcriptomics identifies ergothioneine as a mitochondrial protector to prevent AKI-to-CKD progression.PloS one · 2026Article
- SSO targets CD36 to regulate lipid metabolism disorders and improve SiOCurrent research in toxicology · 2026Article
- Growth hormone-releasing peptide 6 (GHRP-6) hydrogel for acute kidney injury therapy via metabolic regulation.Journal of nanobiotechnology · 2025Article
- Renal tubular epithelial IGFBP7 interacts with PKM2 to drive renal lipid accumulation and fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Association between the atherogenic index of plasma and mortality in the chronic kidney disease population: evidence from NHANES.Frontiers in medicine · 2025Article
- Identification of key lipid metabolism-related genes in kidney fibrosis: implications for chronic kidney disease management.Frontiers in physiology · 2025Article
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13 authors.
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Abstract
Acute kidney injury (AKI) can progress to chronic kidney disease (CKD) and subsequently to renal fibrosis. Poor repair of renal tubular epithelial cells (TECs) after injury is the main cause of renal fibrosis. Studies have shown that restoring damaged fatty acid β-oxidation (FAO) can reduce renal fibrosis. Adipose triglyceride lipase (ATGL) is a key enzyme that regulates lipid hydrolysis. This study, for the first time, demonstrated that ATGL was downregulated in the renal TEC in the AKI-CKD transition mouse model. Moreover, treatment with the ATGL inhibitor atglistatin exacerbated lipid accumulation and downregulated the FAO level and mitochondrial function, while it increased the level of oxidative stress injury and apoptosis, resulting in aggravated renal fibrosis. In contrast, ATGL overexpression suppressed lipid accumulation, improved the FAO level and mitochondrial function, and attenuated oxidative stress and apoptosis, thereby ameliorating fibrosis in vitro and in vivo. In summary, ATGL regulates renal fibrosis by reprogramming lipid metabolism in renal TECs. This study provided new avenues and targets for treating CKD.
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