The roles of endothelin and its receptors in cigarette smoke-associated pulmonary hypertension with chronic lung disease.
Pathol Res Pract
; 216(9): 153083, 2020 Sep.
Article
en En
| MEDLINE
| ID: mdl-32825951
Chronic exposure to cigarette smoke is the major risk factor for the development of pulmonary hypertension (PH) with chronic lung disease (i.e. PH group III). The pathogenesis of smoke-associated PH group III in chronic obstructive pulmonary disease (COPD) involves cigarette smoke exposure-induced damage to lung tissue and dysfunction of pulmonary system with increased synthesis and release of endothelin-1 (ET-1), hypoxia, inflammation, pulmonary vascular remodeling. Many studies have demonstrated that cigarette smoke exposure induces activation of mitogen-activated protein kinase (MAPK) signal pathway that leads to up-regulation of ET-1 and its receptors with the receptor-mediated enhanced contraction, proliferation of pulmonary vascular smooth muscle cells, pulmonary vascular remodeling, elevated pulmonary arterial pressure and finally PH group III. This mini-review article aims to summarize the current state of understanding on the roles of cigarette smoke-induced up-regulation of ET-1 and its receptors in the development of PH group III. Understanding the underlying molecular mechanisms that cigarette smoke exposure leads to PH group III may provide a novel strategy for the treatment.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Hipertensión Pulmonar
/
Pulmón
/
Enfermedades Pulmonares
/
Músculo Liso Vascular
Tipo de estudio:
Risk_factors_studies
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Pathol Res Pract
Año:
2020
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Alemania