What question did this study set out to answer?

The research aims to explore how METTL14 influences lipid metabolism and atherogenesis through PPAR-α/γ expression.

March 26, 2026Open Access

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

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

Population

Vascular smooth muscle cells (VSMCs) and preclinical models of atherosclerosis

Intervention

METTL14

Outcome

Atherogenesis and lipid metabolismsurrogate

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

Main Result

Absolute Event Rate: 0% vs 0%

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.