| Literature DB >> 29351435 |
Qing Lu1,2, Eric Gottlieb2, Sharon Rounds1,2.
Abstract
Cigarette smoking is the leading cause of preventable disease and death in the United States. Cardiovascular comorbidities associated with both active and secondhand cigarette smoking indicate the vascular toxicity of smoke exposure. Growing evidence supports the injurious effect of cigarette smoke on pulmonary endothelial cells and the roles of endothelial cell injury in development of acute respiratory distress syndrome (ARDS), emphysema, and pulmonary hypertension. This review summarizes results from studies of humans, preclinical animal models, and cultured endothelial cells that document toxicities of cigarette smoke exposure on pulmonary endothelial cell functions, including barrier dysfunction, endothelial activation and inflammation, apoptosis, and vasoactive mediator production. The discussion is focused on effects of cigarette smoke-induced endothelial injury in the development of ARDS, emphysema, and vascular remodeling in chronic obstructive pulmonary disease.Entities:
Keywords: acute respiratory distress syndrome; cigarette smoke; emphysema; endothelial cells; pulmonary hypertension
Mesh:
Year: 2018 PMID: 29351435 PMCID: PMC6008130 DOI: 10.1152/ajplung.00373.2017
Source DB: PubMed Journal: Am J Physiol Lung Cell Mol Physiol ISSN: 1040-0605 Impact factor: 5.464