Abstract:
The demethylase fat mass and obesity-associated protein (FTO) is the first discovered N
6-methyladenosine (m
6A) demethylase, serving as a critical “eraser” in m
6A methylation regulation. By dynamically modulating RNA epigenetic modifications, FTO plays a key role in maintaining methylation equilibrium. Emerging evidence highlights the significance of m
6A methylation in cardiovascular disease (CVD) pathogenesis, influencing various pathophysiological processes. Studies suggest that FTO-mediated m
6A demethylation contributes to CVD progression, positioning FTO as a potential therapeutic target. This review systematically examines FTO’s molecular structure, its function in m
6A modification, and its regulatory mechanisms in CVD, including genetic variations. Additionally, we explore FTO’s therapeutic implications across different CVD subtypes, offering insights into future research directions.