m⁶A in adipose tissue inflammation: A novel regulator of obesity and metabolic diseases (Review)

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Adipose tissue hypertrophy, the local infiltration of immune cells, the increased production of proinflammatory cytokines, the whitening of brown adipose tissue, local hypoxia and angiogenesis disorders occur in obese individuals, which in turn lead to adipose tissue inflammation and promote the occurrence and development of metabolic diseases such as type 2 diabetes (T2DM), atherosclerosis and metabolic dysfunction‑associated steatotic liver disease (MASLD). In recent years, N6‑methyladenine (m 6 A), the most representative epigenetic modification, has been shown to be significantly altered in individuals with obesity and to participate in the regulation of various metabolic diseases. In the present review, the links between m6A modification and obesity‑related metabolic diseases, such as MASLD and T2DM, from the perspective of adipose tissue inflammation are examined. Additionally, the challenges and prospects associated with targeting m6A in adipose tissue inflammation and metabolic diseases are discussed to provide new ideas for the treatment of these conditions.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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