Ying-Huizi Shen, Dong Ding, Tian-Yu Lian, Bao-Chen Qui, Yi Yan, Pei-Wen Wang, Wei-Hua Zhang, Zhi-Cheng Jing
First Hospital of Jilin University. Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College. Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Southern Medical University. Shanghai Children’s Medical Center, National Children’s Medical Center and Shanghai Jiao Tong University School of Medicine.
China
Journal of Molecular and Cellular Cardiology
J Mol Cell Cardiol 2024;
DOI: 10.1016/j.yjmcc.2024.10.004
Abstract
Pulmonary arterial hypertension (PAH) is a fatal lung disease characterized by progressive pulmonary vascular remodeling. The initial cause of pulmonary vascular remodeling is the dysfunction of pulmonary arterial endothelial cells (PAECs), manifested by changes in the categorization of cell subtypes, endothelial programmed cell death, such as apoptosis, necroptosis, pyroptosis, ferroptosis, et al., overproliferation, senescence, metabolic reprogramming, endothelial-to-mesenchymal transition, mechanosensitivity, and regulation ability of peripheral cells. Therefore, it is essential to explore the mechanism of endothelial dysfunction in the context of PAH. This review aims to provide a comprehensive understanding of the molecular mechanisms underlying endothelial dysfunction in PAH. We highlight the developmental process of PAECs and changes in PAH and summarise the latest classification of endothelial dysfunction. Our review could offer valuable insights into potential novel EC-specific targets for preventing and treating PAH.
Category
Vascular Cell Biology and Mechanisms of Pulmonary Vascular Disease
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