ArticleAmerican journal of physiology. Cell physiology2025
The role of carnitine palmitoyl transferase 2 in the progression of salt-sensitive hypertension.
Article in American journal of physiology. Cell physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Metabolic hubs in reproduction: The regulatory network of lipid droplets in gamete and embryo physiology (Review).International journal of molecular medicine · 2026Review
- Transcriptomic insights into aerobic exercise-mediated attenuation of high-fat diet-induced muscle wasting.Frontiers in physiology · 2026Article
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12 authors.
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Abstract
Carnitine palmitoyl transferase 2 (CPT2) is a key enzyme in mitochondrial fatty acid oxidation (FAO), a process critical for renal energy homeostasis. Disruption of FAO and accumulation of plasma acylcarnitines (fatty acids conjugated to carnitine) have been implicated in renal and vascular diseases. Although the kidney relies heavily on FAO, the specific renal consequences of CPT2 deficiency remain poorly understood. Clinical data suggest that CPT2 expression may be associated with increased lifespan in patients on antihypertensive therapy, yet a direct link between CPT2 and hypertension has not been established. Our previous work in salt-sensitive (SS) hypertension showed that a high-salt (HS) diet increases FAO while reducing renal acylcarnitine levels. To investigate how CPT2 deficiency affects renal function and metabolic regulation under dietary stress, we generated a novel CPT2-deficient rat model on the Dahl SS background. Homozygous knockouts were embryonically lethal; thus, heterozygous (
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