ArticleCell death & disease2021
CPT1α maintains phenotype of tubules via mitochondrial respiration during kidney injury and repair.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Metabolic control by liver-kidney crosstalk and glucagon in health and disease.Nature reviews. Nephrology · 2026Review
- Mitochondrial dysfunction of renal tubular epithelial cells in chronic kidney disease-associated fibrosis: from organelle homeostasis to multicellular remodeling.Molecular biology reports · 2026Review
- Redox-Mediated Mitochondrial Dysfunction as a Common Pathogenic Axis in Acute Kidney Injury and Chronic Kidney Disease.Biomolecules · 2026Review
- High-Dose Aluminium Chloride Exposure Disrupts the Renal Cortical Injury-Repair Balance in Rats: Partial Modulation by L-Carnitine Pretreatment.Animals : an open access journal from MDPI · 2026Article
- Therapeutic remodeling of the ceramide backbone prevents kidney injury.Cell metabolism · 2026Article
- Kidney organoids as a novel platform to evaluate heat-stress-induced acute kidney injury pathogenesis.Bioengineering & translational medicine · 2026Article
- Nanoparticle-mediated overexpression of RacGAP1 protects against renal ischemia/reperfusion injury by maintaining mitochondrial homeostasis.Clinical science (London, England : 1979) · 2025Article
- SIRT3 regulates CPT1a acetylation and fatty acid oxidation in renal tubular epithelial cells under diabetic condition.Molecular biology reports · 2025Article
- How the Renal Tubule May Adapt to Fuel Shortage.Kidney360 · 2025Article
- Zinc Deficiency Causes Glomerulosclerosis and Renal Interstitial Fibrosis Through Oxidative Stress and Increased Lactate Metabolism in Rats.Biological trace element research · 2025Article
- Sulforaphane Restores Mitochondrial β-Oxidation and Reduces Renal Lipid Accumulation in a Model of Releasing Unilateral Ureteral Obstruction.Antioxidants (Basel, Switzerland) · 2025Article
- Integrin-Linked Kinase (ILK) Promotes Mitochondrial Dysfunction by Decreasing CPT1A Expression in a Folic Acid-Based Model of Kidney Disease.International journal of molecular sciences · 2025Article
- Baicalin: a potential therapeutic agent for acute kidney injury and renal fibrosis.Frontiers in pharmacology · 2025Review
- Cpt1a Drives primed-to-naïve pluripotency transition through lipid remodeling.Communications biology · 2024Article
- PAR2-mediated cellular senescence promotes inflammation and fibrosis in aging and chronic kidney disease.Aging cell · 2024Article
- Article
- VNS improves VSMC metabolism and arteriogenesis in infarcted hearts through m/n-AChR-Akt-SDF-1α in adult male rats.Journal of molecular histology · 2024Article
- Ischemic tubular injury: Oxygen-sensitive signals and metabolic reprogramming.Inflammopharmacology · 2023Review
- Direct mapping of kidney function by DCE-MRI urography using a tetrazinanone organic radical contrast agent.Nature communications · 2023Article
- Metabolic reprogramming heterogeneity in chronic kidney disease.FEBS open bio · 2023Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Impaired energy metabolism in proximal tubular epithelial cells (PTECs) is strongly associated with various kidney diseases. Here, we characterized proximal tubular phenotype alternations during kidney injury and repair in a mouse model of folic acid nephropathy, in parallel, identified carnitine palmitoyltransferase 1α (CPT1α) as an energy stress response accompanied by renal tubular dedifferentiation. Genetic ablation of Cpt1α aggravated the tubular injury and interstitial fibrosis and hampered kidney repair indicate that CPT1α is vital for the preservation and recovery of tubular phenotype. Our data showed that the lipid accumulation and mitochondrial mass reduction induced by folic acid were persistent and became progressively more severe in PTECs without CPT1α. Interference of CPT1α reduced capacities of mitochondrial respiration and ATP production in PTECs, and further sensitized cells to folic acid-induced phenotypic changes. On the contrary, overexpression of CPT1α protected mitochondrial respiration and prevented against folic acid-induced tubular cell damage. These findings link CPT1α to intrinsic mechanisms regulating the mitochondrial respiration and phenotype of kidney tubules that may contribute to renal pathology during injury and repair.
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