ArticleThe Journal of clinical investigation2021
Renal tubule Cpt1a overexpression protects from kidney fibrosis by restoring mitochondrial homeostasis.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 208 papers, 2 of them syntheses that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
208 citing papers in PubMed, 2 syntheses or guidelines pooled it, 322 citations in OpenAlex.
- Lipid Peroxidation in Diabetic Kidney Disease: Mechanism and Natural Solution.International journal of molecular sciences · 2025Pooled it
- Lipid homeostasis in diabetic kidney disease.International journal of biological sciences · 2024Pooled it
- Involvement of impaired carnitine-induced fatty acid oxidation in experimental and human diabetic kidney disease.JCI insight · 2025Trial
- Ligustroflavone alleviates chronic kidney disease by inhibiting ferroptosis through the GSK3β/NRF2 signaling pathway.Redox report : communications in free radical research · 2026Article
- Ginsenoside Rg3 attenuates hyperuricemia-associated AKI by upregulating CPT1A and suppressing NLRP3/Caspase-1/GSDMD-mediated pyroptosis.In vitro cellular & developmental biology. Animal · 2026Article
- Shared inflammatory-metabolic transcriptional effects in tubulointerstitial fibrosis and clear cell renal cell carcinoma.Translational oncology · 2026Article
- Mitochondrial dysfunction of renal tubular epithelial cells in chronic kidney disease-associated fibrosis: from organelle homeostasis to multicellular remodeling.Molecular biology reports · 2026Review
- Adipose Mesenchymal Stem Cells Secreted Exosomal miR-26a-5p Ameliorate Renal Fibrosis via Inhibiting Glycolysis and Ferroptosis in Renal Interstitial Fibrosis.Journal of cellular and molecular medicine · 2026Article
- Disulfiram Attenuates Adenine-Induced Renal Fibrosis by Modulating Inflammatory and Immunometabolic Responses.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- SOCS2 Downregulation Is Associated with a Ferro-Aging-Related Transcriptomic Signature in Proximal Tubular Cells in Chronic Kidney Disease.Biomedicines · 2026Article
- STAT3 suppresses palmitic acid-induced apoptosis and fatty acid oxidation dysfunction in bovine mammary epithelial cells by transcriptionally activating CPT1A.Science China. Life sciences · 2026Article
- Twist Family BHLH Transcription Factor 1 orchestrates hypoxia-lactate crosstalk to bridge glycolytic flux and tubular maladaptation in fibrotic kidneys.Molecular biomedicine · 2026Article
- Endogenous Lipid Signals in Energy Homeostasis and Fibrosis.Biomolecules · 2026Review
- SLC38A6 expression in renal tubular cells accelerates cisplatin-induced acute kidney injury by promoting cell apoptosis.The FEBS journal · 2026Article
- Depletion and replacement of tissue-resident macrophages in mice with germ-line deletion of a conserved enhancer in the Csf1r locus.Development (Cambridge, England) · 2026Article
- Review
- Peroxisomal Degradation Correlates with the Progression of Kidney Injury in a UUO Mouse Model.Biology · 2026Article
- Magnesium as a Bioenergetic Checkpoint Linking Mitochondrial Function, Metabolic Disease, and Aging.Aging cell · 2026Review
- Glycolytic lactylation modulates cell death decisions in diabetic kidney disease: Metabolic‑epigenetic interplay between ferroptosis and autophagy in fibrotic remodeling (Review).International journal of molecular medicine · 2026Review
- Cold atmospheric plasma ameliorating skin barrier in chronic kidney disease.NPJ Regenerative medicine · 2026Article
148 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
19 authors at 9 institutions in 3 countries.
Funding
Abstract
Chronic kidney disease (CKD) remains a major epidemiological, clinical, and biomedical challenge. During CKD, renal tubular epithelial cells (TECs) present a persistent inflammatory and profibrotic response. Fatty acid oxidation (FAO), the main source of energy for TECs, is reduced in kidney fibrosis and contributes to its pathogenesis. To determine whether gain of function in FAO (FAO-GOF) could protect from fibrosis, we generated a conditional transgenic mouse model with overexpression of the fatty acid shuttling enzyme carnitine palmitoyl-transferase 1A (CPT1A) in TECs. Cpt1a-knockin (CPT1A-KI) mice subjected to 3 models of renal fibrosis (unilateral ureteral obstruction, folic acid nephropathy [FAN], and adenine-induced nephrotoxicity) exhibited decreased expression of fibrotic markers, a blunted proinflammatory response, and reduced epithelial cell damage and macrophage influx. Protection from fibrosis was also observed when Cpt1a overexpression was induced after FAN. FAO-GOF restored oxidative metabolism and mitochondrial number and enhanced bioenergetics, increasing palmitate oxidation and ATP levels, changes that were also recapitulated in TECs exposed to profibrotic stimuli. Studies in patients showed decreased CPT1 levels and increased accumulation of short- and middle-chain acylcarnitines, reflecting impaired FAO in human CKD. We propose that strategies based on FAO-GOF may constitute powerful alternatives to combat fibrosis inherent to CKD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.