The roles of endothelin and its receptors in cigarette smoke-associated pulmonary hypertension with chronic lung disease |
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Institution: | 1. Department of Anesthesiology, The 2nd Affiliated Hospital of Harbin Medical University, Harbin 150086, China;2. Department of General Surgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin 150086, China;1. Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing, Jiangsu 210009, PR China;2. Department of Environmental Occupational Health, Taizhou Center for Disease Control and Prevention, No.318 Yongtai Road, Hailing District, Taizhou City, Jiangsu Province, PR China;1. Department of Microbiology, Kashan University of Medical Sciences, Kashan, Iran;2. Department of Biochemistry and Nutrition, Research Center for Evidence-Based Health Management, Maragheh University of Medical Sciences, Maragheh, Iran;3. Research Center for Biochemistry and Nutrition in Metabolic Diseases, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, Iran |
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Abstract: | 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. |
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Keywords: | endothelin-1 Receptor MAPK PH group III Cigarette smoke exposure |
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