Related Experiment Video
Updated: Aug 9, 2025

Author Spotlight: Exploring the Relationship Between Lipotoxicity and HFpEF
Published on: March 29, 2024
L-carnitine attenuated hyperuricemia-associated left ventricular remodeling through ameliorating cardiomyocytic lipid
Yang Yang1,2,3, Cuiting Lin3, Qiang Zheng3
1Affiliated Foshan Maternity & Child Healthcare Hospital, Southern Medical University, Foshan, Guangdong, China.
Insights
High uric acid (HUA) impairs heart cell fatty acid (FA) metabolism, causing cardiac remodeling. L-carnitine (LC) treatment improves FA transport and reduces heart damage, offering a potential therapy for HUA-related cardiovascular disease.
Area of Science:
- Cardiology
- Metabolic Disorders
- Molecular Biology
Background:
- Hyperuricemia (HUA) is linked to left ventricular remodeling (LVR) and cardiovascular diseases.
- Left ventricular remodeling involves cardiomyocyte energy metabolic dysfunction.
- The impact of HUA on cardiomyocyte fatty acid (FA) metabolism remains largely unknown.
Purpose of the Study:
- To investigate the effect of HUA on cardiomyocyte FA metabolism.
- To explore the therapeutic potential of L-carnitine (LC) in HUA-associated cardiac dysfunction.
Main Methods:
- Utilized a mouse model of HUA.
- Assessed cardiomyocyte injury and lipid deposition.
- Investigated the role of carnitine palmitoyl transferase 1B (CPT1B) in FA transport.
- Evaluated the effects of L-carnitine (LC) intervention.
Main Results:
- Uric acid (UA) induces cardiomyocyte injury and cytoplasmic lipid accumulation.
- UA suppresses CPT1B, inhibiting mitochondrial FA transport.
- LC treatment ameliorates UA-induced cardiac lipid deposition and LVR.
- LC intervention reduced left ventricular anterior wall thickening in HUA mice.
Conclusions:
- FA transport dysfunction is a key mechanism in HUA-induced cardiomyocytic injury and LVR.
- Promoting FA transport via LC is a viable therapeutic strategy for HUA-associated LVR.
- Targeting FA metabolism offers a novel approach to managing cardiovascular complications of HUA.
Abstract:
Hyperuricemia (HUA) is associated with left ventricular remodeling (LVR) and thereby causes the initiation and development of a large number of cardiovascular diseases. LVR is typically accompanied by cardiomyocyte energy metabolic disorder. The energy supply of cardiomyocytes is provided by glucose and fatty acid (FA) metabolism. Currently, the effect of HUA on cardiomyocytic FA metabolism is unclear. In this study, we demonstrate that UA-induced cardiomyocyte injury is associated with cytoplasmic lipid deposition, which can be ameliorated by the FA metabolism-promoting drug L-carnitine (LC). UA suppresses carnitine palmitoyl transferase 1B (CPT1B), thereby inhibiting FA transport into the mitochondrial inner matrix for elimination. LC intervention can ameliorate HUA-associated left ventricular anterior wall thickening in mice. This study showed that FA transport dysfunction plays is a critical mechanism in both cardiomyocytic injury and HUA-associated LVR and promoting cytoplasmic FA transportation through pharmacological treatment by LC is a valid strategy to attenuate HUA-associated LVR.
Related Concept Videos
Cardiomyopathy V: Interprofessional Care
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Lipid-Lowering Drugs: Statins and Miscellaneous Agents
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Cardiomyopathy II: Dilated Cardiomyopathy
Atherosclerosis III: Management

