RNA m6A methylation and regulatory proteins in pulmonary arterial hypertension

Zhe Wang, Yi-Xuan Zhang, Jun-Zhuo Shi, Yi Yan, Lu-Ling Zhao, Jie-Jian Kou, Yang-Yang He, Xin-Mei Xie, Si-Jin Zhang, Xiao-Bin Pang
Huaihe Hospital of Henan University. Shanghai Children’s Medical Center, National Children’s Medical Center and Shanghai Jiao Tong University School of Medicine. Guangdong Provincial People’s Hospital and Southern Medical University.
China

Hypertension Research
Hypertens Res 2024;
DOI: 10.1038/s41440-024-01607-9

Abstract
m6A (N6‑methyladenosine) is the most common and abundant apparent modification in mRNA of eukaryotes. The modification of m6A is regulated dynamically and reversibly by methyltransferase (writer), demethylase (eraser), and binding protein (reader). It plays a significant role in various processes of mRNA metabolism, including regulation of transcription, maturation, translation, degradation, and stability. Pulmonary arterial hypertension (PAH) is a malignant cardiopulmonary vascular disease characterized by abnormal proliferation of pulmonary artery smooth muscle cells. Despite the existence of several effective and targeted therapies, there is currently no cure for PAH and the prognosis remains poor. Recent studies have highlighted the crucial role of m6A modification in cardiovascular diseases. Investigating the role of RNA m6A methylation in PAH could provide valuable insights for drug development. This review aims to explore the mechanism and function of m6A in the pathogenesis of PAH and discuss the potential targeting of RNA m6A methylation modification as a treatment for PAH.

Category
Vascular Cell Biology and Mechanisms of Pulmonary Vascular Disease
Animal Models of Pulmonary Vascular Disease and Therapy
Review Articles Concerning Pulmonary Vascular Disease

Age Focus: Pediatric Pulmonary Vascular Disease or Adult Pulmonary Vascular Disease

Fresh or Filed Publication: Fresh (PHresh). Less than 1-2 years since publication

Article Access
Free PDF File or Full Text Article Available Through PubMed or DOI: No

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