The Role of N(6)-Methyladenosine Modification in Microvascular Dysfunction

Microvascular dysfunction (MVD) has long plagued the medical field despite improvements in its prevention, diagnosis, and intervention. Microvascular lesions from MVD increase with age and further lead to impaired microcirculation, target organ dysfunction, and a mass of microvascular complications, thus contributing to a heavy medical burden and rising disability rates. An up-to-date understanding of molecular mechanisms underlying MVD will facilitate discoveries of more effective therapeutic strategies. Recent advances in epigenetics have revealed that RNA methylation, an epigenetic modification, has a pivotal role in vascular events. The N(6)-methylation of adenosine (m(6)A) modification is the most prevalent internal RNA modification in eukaryotic cells, which regulates vascular transcripts through splicing, degradation, translation, as well as translocation, thus maintaining microvascular homeostasis. Conversely, the disruption of the m(6)A regulatory network will lead to MVD. Herein, we provide a review discussing how m(6)A methylation interacts with MVD. We also focus on alterations of the m(6)A regulatory network under pathological conditions. Finally, we highlight the value of m(6)A regulators as prognostic biomarkers and novel therapeutic targets, which might be a promising addition to clinical medicine.