m6A modification on ncRNAs and underlying mechanisms of exercise in the regulation of pathological cardiac remodeling

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)

Cardiovascular diseases are a significant menace to human health and life, with pathological cardiac remodeling being a pivotal phase in a spectrum of cardiovascular conditions. In recent years, within the field of epigenetic modifications, N6-methyladenosine (m6A) has risen to prominence as a dynamic and reversible form of RNA methylation. This modification has been shown to modulate the transmission of various signaling pathways and is integral to the pathological remodeling processes of the heart. Advances in molecular biology and the emergence of high-throughput sequencing technologies have facilitated the identification of numerous m6A methylation sites on non-coding RNAs (ncRNAs). These epigenetic alterations have been correlated with a myriad of diseases, notably those associated with cardiac remodeling. Studies have indicated that moderate exercise training can modulate m6A methylation and ncRNA levels across different disease models. Consequently, the aim of this review is to delve into the molecular mechanisms by which m6A methylation affects ncRNAs and to explore the potential pathways through which exercise might exert its influence on the progression of pathological cardiac remodeling. Gaining this insight could uncover novel research targets and pave the way for innovative diagnostic and therapeutic strategies in the management of pathological cardiac remodeling.

Evidence level

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

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