Amir Tajbakhsh, Seyed Mohammad Gheibihayat, Deniz Mortazavi, Pourya Medhati, Behrouz Rostami, Amir Savardashtaki, Amir Abbas Momtazi-Borojeni
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引用次数: 5
Abstract
Cigarette smoking-related inflammation, cellular stresses, and tissue destruction play a key role in lung disease, such as chronic obstructive pulmonary disease (COPD). Notably, augmented apoptosis and impaired clearance of apoptotic cells, efferocytosis, contribute to the chronic inflammatory response and tissue destruction in patients with COPD. Of note, exposure to cigarette smoke can impair alveolar macrophages efferocytosis activity, which leads to secondary necrosis formation and tissue inflammation. A better understanding of the processes behind the effect of cigarette smoke on efferocytosis concerning lung disorders can help to design more efficient treatment approaches and also delay the development of lung disease, such as COPD. To this end, we aimed to seek mechanisms underlying the impairing effect of cigarette smoke on macrophages-mediated efferocytosis in COPD. Further, available therapeutic opportunities for restoring efferocytosis activity and ameliorating respiratory tract inflammation in smokers with COPD were also discussed.
期刊介绍:
From pathophysiology and cell biology to pharmacology and psychosocial impact, COPD: Journal Of Chronic Obstructive Pulmonary Disease publishes a wide range of original research, reviews, case studies, and conference proceedings to promote advances in the pathophysiology, diagnosis, management, and control of lung and airway disease and inflammation - providing a unique forum for the discussion, design, and evaluation of more efficient and effective strategies in patient care.