Role of prostanoids, nitric oxide and endothelin pathways in pulmonary hypertension due to COPD

Frontiers in Medicine

Medicine

Rayan A. Siraj¹  Jaber S. Alqahtani²  Abdullah A. Alqarni³  Saad M. Alshehri⁴  Hassan Alwafi⁵  Abdulkareem A. AlGarni⁶  Mansour S. Majrshi⁷  Sara A. Alghamdi⁸  Linhua Pang⁹  Abdulelah M. Aldhahir^1,10 

[1] Department of Respiratory Care, College of Applied Medical Sciences, King Faisal University, Al Ahsa, Saudi Arabia;Department of Respiratory Care, Prince Sultan Military College of Health Sciences, Dammam, Saudi Arabia;Department of Respiratory Therapy, Faculty of Medical Rehabilitation Sciences, King Abdulaziz University, Jeddah, Saudi Arabia;Respiratory Therapy Unit, King Abdulaziz University Hospital, Jeddah, Saudi Arabia;Department of Respiratory Therapy, King Fahad General Hospital, Jeddah, Saudi Arabia;Faculty of Medicine, Umm Al-Qura University, Mecca, Saudi Arabia;King Abdulaziz Hospital, The Ministry of National Guard Health Affairs, Al Ahsa, Saudi Arabia;King Saud bin Abdulaziz University for Health Sciences, College of Applied Medical Sciences, Al Ahsa, Saudi Arabia;National Heart and Lung Institute, Imperial College London, London, United Kingdom;Respiratory Medicine, Royal Brompton Hospital, London, United Kingdom;Respiratory Care Department, Al Murjan Hospital, Jeddah, Saudi Arabia;Respiratory Medicine Research Group, Academic Unit for Translational Medical Sciences, University of Nottingham School of Medicine, Nottingham, United Kingdom;Respiratory Therapy Department, Faculty of Applied Medical Sciences, Jazan University, Jazan, Saudi Arabia;

关键词: nitric oxide;    prostanoid;    pulmonary hypertension;    COPD;    endothelin;    type 3 pulmonary hypertension;    COPD-associated pulmonary hypertension;    pulmonary hypertension in COPD;   

DOI  :  10.3389/fmed.2023.1275684

 received in 2023-08-10, accepted in 2023-09-19,  发布年份 2023

来源: Frontiers

【 摘 要 】

Pulmonary hypertension (PH) due to chronic obstructive pulmonary disease (COPD) is classified as Group 3 PH, with no current proven targeted therapies. Studies suggest that cigarette smoke, the most risk factor for COPD can cause vascular remodelling and eventually PH as a result of dysfunction and proliferation of pulmonary artery smooth muscle cells (PASMCs) and pulmonary artery endothelial cells (PAECs). In addition, hypoxia is a known driver of pulmonary vascular remodelling in COPD, and it is also thought that the presence of hypoxia in patients with COPD may further exaggerate cigarette smoke-induced vascular remodelling; however, the underlying cause is not fully understood. Three main pathways (prostanoids, nitric oxide and endothelin) are currently used as a therapeutic target for the treatment of patients with different groups of PH. However, drugs targeting these three pathways are not approved for patients with COPD-associated PH due to lack of evidence. Thus, this review aims to shed light on the role of impaired prostanoids, nitric oxide and endothelin pathways in cigarette smoke- and hypoxia-induced pulmonary vascular remodelling and also discusses the potential of using these pathways as therapeutic target for patients with PH secondary to COPD.

【 授权许可】

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Copyright © 2023 Alqarni, Aldhahir, Alghamdi, Alqahtani, Siraj, Alwafi, AlGarni, Majrshi, Alshehri and Pang.