ArticleThe Journal of surgical research2012
Stimulation of carnitine palmitoyltransferase 1 improves renal function and attenuates tissue damage after ischemia/reperfusion.
Article in The Journal of surgical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 53 citations in OpenAlex.
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- Altered Carnitine Homeostasis Modulates Hyperosmolarity-Induced Mitochondrial Dysfunction and Lipotoxicity in Human Corneal Epithelial Cells.Investigative ophthalmology & visual science · 2026Article
- Therapeutic remodeling of the ceramide backbone prevents kidney injury.Cell metabolism · 2026Article
- The role of carnitine palmitoyl transferase 2 in the progression of salt-sensitive hypertension.American journal of physiology. Cell physiology · 2025Article
- Intracellular pH links energy metabolism to lymphocyte death and proliferation.Scientific reports · 2025Article
- DNA damage in proximal tubules triggers systemic metabolic dysfunction through epigenetically altered macrophages.Nature communications · 2025Article
- Article
- Extreme Heat Exposure Induced Acute Kidney Injury through NLRP3 Inflammasome Activation in Mice.Environment & health (Washington, D.C.) · 2024Article
- Article
- The Physiological and Pathological Role of Acyl-CoA Oxidation.International journal of molecular sciences · 2023Review
- New Pathway for Cisplatin Prodrug to Utilize Metabolic Substrate Preference to Overcome Cancer Intrinsic Resistance.ACS central science · 2023Article
- Transcriptional regulation of proximal tubular metabolism in acute kidney injury.Pediatric nephrology (Berlin, Germany) · 2023Review
- Mitochondrial CPT1A: Insights into structure, function, and basis for drug development.Frontiers in pharmacology · 2023Review
- Crosstalk between proximal tubular epithelial cells and other interstitial cells in tubulointerstitial fibrosis after renal injury.Frontiers in endocrinology · 2023Review
- Energy metabolic reprogramming regulates programmed cell death of renal tubular epithelial cells and might serve as a new therapeutic target for acute kidney injury.Frontiers in cell and developmental biology · 2023Review
- Expression Profiles of Kidney Mitochondrial Proteome during the Progression of the Unilateral Ureteral Obstruction: Focus on Energy Metabolism Adaptions.Metabolites · 2022Article
- Tubular Mitochondrial Dysfunction, Oxidative Stress, and Progression of Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
- An Integrated Proteomics and Metabolomics Strategy for the Mechanism of Calcium Oxalate Crystal-Induced Kidney Injury.Frontiers in medicine · 2022Article
- CPT1α maintains phenotype of tubules via mitochondrial respiration during kidney injury and repair.Cell death & disease · 2021Article
- The role of metabolic reprogramming in tubular epithelial cells during the progression of acute kidney injury.Cellular and molecular life sciences : CMLS · 2021Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundRenal injury as a result of ischemia/reperfusion (I/R) is a major clinical problem with a high mortality rate and a lack of therapeutic treatment. During I/R, cellular homeostasis is disrupted owing to energy depletion, leading to cell death. Fatty acid β-oxidation is the major metabolic pathway for generating adenosine triphosphate (ATP) in the kidneys, which is governed by carnitine palmitoyltransferase 1 (CPT1). C75 is a synthetic compound that up-regulates CPT1 activity. Thus, we hypothesized that C75 treatment could increase energy production and alleviate renal I/R injury.
methodsWe subjected male adult rats to renal I/R by bilateral renal pedicle clamping with microvascular clips for 60 min, followed by administration of 8% dimethyl sulfoxide (vehicle) or C75 (3 mg/kg body weight), with 5 animals/group. We collected blood and renal tissues 24 h after reperfusion and subjected them to various measurements and histological examination.
resultsC75 treatment restored the loss of CPT1 activity and intracellular ATP levels in the kidneys after I/R. Administration of C75 significantly lowered serum creatinine, blood urea nitrogen, aspartate aminotransferase, and lactate dehydrogenase levels elevated by I/R. C75 treatment preserved morphological features of the kidneys with a significant improvement in the damage score. In addition, C75 treatment inhibited the increase of TNF-α levels in serum and kidneys, and lowered myeloperoxidase activity in the kidneys after I/R.
conclusionsStimulation of CPT1 activity by C75 recovered ATP depletion, improved renal function, attenuated tissue injury, and inhibited proinflammatory cytokine production and neutrophil infiltration after renal I/R injury. Therefore, enhancing the metabolism pathways for energy production may provide a novel modality to treat renal I/R injury.
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