Targeting <scp> m ⁶ A </scp> Modifications Regulating Ferroptosis Offers Novel Therapy in Diseases

ABSTRACT Ferroptosis, a regulated form of cell death driven by iron‐dependent lipid peroxidation, emerged as a critical process in the pathogenesis of various diseases, including neurological, cardiovascular, hepatic, pulmonary, and renal disorders. Simultaneously, N6‐methyladenosine (m 6 A), the most abundant reversible RNA modification in eukaryotes, plays a pivotal role in gene regulation by modulating RNA stability, translation, and degradation. Evidence increasingly links m 6 A modifications to the transcriptional and post‐transcriptional regulation of ferroptosis, highlighting their importance in disease mechanisms. This review explores the molecular mechanisms underpinning m 6 A modifications and ferroptosis, detailing their interactions in disease progression. Additionally, it evaluates the therapeutic promise of targeting m 6 A regulators to modulate ferroptosis, offering novel approaches for managing diseases with diverse etiologies. By clarifying the role of m 6 A in ferroptosis, this review underscores the promise of m 6 A‐focused therapeutic strategies in advancing treatment for diseases where ferroptosis plays a key pathological role.