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March 26, 2026Cardiovascular Research2 citationsOpen Access

METTL14 inhibits atherogenesis by epigenetically activating PPAR-α/γ transcription and fatty acid oxidation in VSMCs

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LCLei CuiUniversity of Technology SydneyCHCheng Kiu HoPLPanhong Liang

Key Result

METTL14 promotes lipid metabolism and inhibits atherogenesis by activating PPAR-α/γ expression and fatty acid oxidation in vascular smooth muscle cells.

Key Points

  • The research aims to explore how METTL14 influences lipid metabolism and atherogenesis through PPAR-α/γ expression.
  • Experimental models were used to assess the effects of METTL14 on PPAR-α/γ expression.
  • Lipid metabolism was evaluated in vascular smooth muscle cells (VSMCs).
  • Atherogenesis was analyzed through physiological assessments of arterial health.
  • METTL14 significantly enhances the expression of PPAR-α/γ.
  • Increased PPAR-α/γ leads to improved fatty acid oxidation.
  • Inhibition of atherogenesis was observed in models with active METTL14.

Structured PICO

P
Population
Vascular smooth muscle cells (VSMCs) and preclinical models of atherosclerosis
I
Intervention
METTL14
O
Outcome
Atherogenesis and lipid metabolismsurrogate

The endogenous METTL14/PPAR-α/γ axis represents a potential therapeutic target for treating atherosclerotic and metabolic diseases.

Abstract

We have unveiled that METTL14 promotes lipid metabolism and inhibits atherogenesis through activating PPAR-α/γ expression. These experiments highlight the therapeutic potential of the endogenous METTL14/PPAR-α/γ axis for treating atherosclerotic and metabolic diseases.

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Cite This Study

Cui et al. (2026) studied this question. METTL14 promotes lipid metabolism and inhibits atherogenesis by activating PPAR-α/γ expression and fatty acid oxidation in vascular smooth muscle cells.

synapsesocial.com/papers/69c4cd49fdc3bde4489196bchttps://doi.org/10.1093/cvr/cvag069
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