ArticleProceedings of the National Academy of Sciences of the United States of America2025
Tubular ACSM3 deficiency impairs medium-chain fatty acid metabolism and aggravates kidney fibrosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Emerging roles of ATP citrate lyase in kidney diseases: from pathogenic driver to therapeutic target.Renal failure · 2026Review
- S100A1 Promotes MDM2-Mediated KLF15 Ubiquitination to Regulate ID1-Driven Tubular Injury in Diabetic Kidney Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Multi-omics-driven precision medicine.iMeta · 2026Review
- Safety and Efficacy Assessment of Cannabis Plant Compared to Atorvastatin for Lipid Lowering in Diabetic and Obese Wistar Male Rats.Life (Basel, Switzerland) · 2026Article
- Tubular ACSM3 controls fatty acid metabolism and safeguards against acute kidney injury in male mice.Nature communications · 2026Article
- Uremic toxins promote renal fatty acid synthesis and fibrosis via activating aryl hydrocarbon receptor.Nature communications · 2026Article
- ACLY-Driven Metabolic Reprogramming Promotes Histone Acetylation and Inflammation-Associated Fibrosis in Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Renal function-improving action of Pentadecyl®, a multifunctional triglyceride fromExperimental and therapeutic medicine · 2026Article
- Dysregulation of the Upb1-3-ureidopropionate Pathway Impairs Fatty Acid Metabolism and Exacerbates Acute Kidney Injury.International journal of biological sciences · 2026Article
- Lipid metabolism drives podocyte injury in diabetic kidney disease.Frontiers in immunology · 2026Review
- Mitophagy and Cellular Homeostasis in Kidney Diseases: Mechanisms and Potential Therapeutics.International journal of biological sciences · 2026Review
- Targeting tubular epithelial cell metabolism to halt renal fibrosis: current evidence and future directions.Frontiers in cell and developmental biology · 2026Review
- Delactylase effects of SIRT3 on a positive feedback loop involving the RUNX1-glycolysis-histone lactylation in diabetic kidney disease.International journal of biological sciences · 2026Article
- Tubular ACSM3 deficiency impairs medium-chain fatty acid metabolism and aggravates kidney fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
Abstract
Kidney fibrosis is driven by multiple factors, among which impaired fatty acid oxidation has emerged as a critical determinant. Acyl-Coenzyme A (CoA) synthetase medium-chain family member 3 (ACSM3), a key enzyme of medium-chain fatty acid (MCFA) metabolism, has been implicated in metabolic syndrome, but its function in fibrotic kidney remains unexplored. Here, we found that tubular epithelial ACSM3 expression was downregulated in kidney fibrotic mice and patients and inversely correlated with disease severity. Systemic and tubular-specific knockout of ACSM3 both exacerbated renal fibrosis, whereas adeno-associated virus (AAV)-mediated ACSM3 overexpression alleviated fibrotic kidneys in mice. Mechanistically, ACSM3 deficiency disrupted MCFA metabolism and resulted in abnormal mitochondrial homeostasis. Notably, we identified that dodecanoic acid (C12:0) could improve kidney fibrosis, which was primarily utilized via ACSM3 in kidneys. Furthermore, C12:0 oxidation impairment caused by tubular ACSM3 deficiency aggravated fibrotic kidney. Together, ACSM3-regulated MCFA metabolism played a pivotal role in kidney fibrosis, highlighting a potent drug target of ACSM3 and a potential supplementary therapy of MCFA against chronic kidney disease.
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