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.

Frontiers in Pharmacology
|February 23, 2023
PubMed

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.

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