The Role of N6-Methyladenosine Modification in Microvascular Dysfunction

Cells. 2022 Oct 11;11(20):3193. doi: 10.3390/cells11203193.

Abstract

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 N6-methylation of adenosine (m6A) 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 m6A regulatory network will lead to MVD. Herein, we provide a review discussing how m6A methylation interacts with MVD. We also focus on alterations of the m6A regulatory network under pathological conditions. Finally, we highlight the value of m6A regulators as prognostic biomarkers and novel therapeutic targets, which might be a promising addition to clinical medicine.

Keywords: N6-methyladenosine modification; angiogenesis; epigenetics; microvascular dysfunctions.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine* / metabolism
  • Biomarkers / metabolism
  • Methylation
  • RNA, Messenger / genetics

Substances

  • RNA, Messenger
  • Adenosine
  • Biomarkers

Grants and funding

This study was supported by National Natural Science Foundation of China (82070974 to X.C., 81970821 and 82271100 to Q.-H.L.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.