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

被引：8

作者：

Alqarni, Abdullah A. ^{[1
,2
]}

Aldhahir, Abdulelah M. ^{[3
]}

Alghamdi, Sara A. ^{[4
]}

Alqahtani, Jaber S. ^{[5
]}

Siraj, Rayan A. ^{[6
]}

Alwafi, Hassan ^{[7
]}

Algarni, Abdulkareem A. ^{[8
,9
]}

Majrshi, Mansour S. ^{[10
,11
]}

Alshehri, Saad M. ^{[12
]}

Pang, Linhua ^{[13
]}

机构：

[1] King Abdulaziz Univ, Fac Med Rehabil Sci, Dept Resp Therapy, Jeddah, Saudi Arabia

[2] King Abdulaziz Univ Hosp, Resp Therapy Unit, Jeddah, Saudi Arabia

[3] Jazan Univ, Fac Appl Med Sci, Resp Therapy Dept, Jazan, Saudi Arabia

[4] Al Murjan Hosp, Resp Care Dept, Jeddah, Saudi Arabia

[5] Prince Sultan Mil Coll Hlth Sci, Dept Resp Care, Dammam, Saudi Arabia

[6] King Faisal Univ, Coll Appl Med Sci, Dept Resp Care, Al Hasa 31982, Saudi Arabia

[7] Umm Al Qura Univ, Fac Med, Mecca, Saudi Arabia

[8] King Abdulaziz Hosp, Minist Natl Guard Hlth Affairs, Al Hasa, Saudi Arabia

[9] King Saud bin Abdulaziz Univ Hlth Sci, Coll Appl Med Sci, Al Hasa, Saudi Arabia

[10] Imperial Coll London, Natl Heart & Lung Inst, London, England

[11] Royal Brompton Hosp, Resp Med, London, England

[12] King Fahad Gen Hosp, Dept Resp Therapy, Jeddah, Saudi Arabia

[13] Univ Nottingham, Acad Unit Translat Med Sci, Sch Med, Resp Med Res Grp, Nottingham NG5 1PB, England

来源：

FRONTIERS IN MEDICINE | 2023年 / 10卷

关键词：

nitric oxide; prostanoid; pulmonary hypertension; COPD; endothelin; type 3 pulmonary hypertension; COPD-associated pulmonary hypertension; pulmonary hypertension in COPD; SMOOTH-MUSCLE-CELLS; RECEPTOR ANTAGONIST BOSENTAN; CIGARETTE-SMOKE EXPOSURE; PROTEIN-KINASE-C; ARTERIAL-HYPERTENSION; PROSTAGLANDIN E-2; CHRONIC HYPOXIA; PROSTACYCLIN ANALOG; BERAPROST SODIUM; DOUBLE-BLIND;

D O I：

10.3389/fmed.2023.1275684

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

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.

引用

页数：13