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Expression of 15-Lipoxygenase and Evidence for Apoptosis in the Lungs From Patients With COPD
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Aortic enlargement in chronic obstructive pulmonary disease (COPD) and emphysema: The Multi-Ethnic Study of Atherosclerosis (MESA) COPD study
2021, International Journal of CardiologyCitation Excerpt :Risk factors for development of aortic aneurysms include factors that increase stress on the aortic wall (e.g. hypertension and elevated diastolic blood pressure), factors that promote degradation of the elastin and collagen fibers within the aorta wall (e.g. aging, smoking, atherosclerosis), and genetic factors that predispose the aortic wall to degeneration (e.g. Marfan syndrome, Ehler-Danlos, Cutis Laxa). Since emphysema also results from destruction of elastin and collagen [34,35], it is not surprising that emphysema is associated with increasing aortic diameters and aortic aneurysms [36]. Tobacco smoke inhibits the anti-elastase activity of alpha1-antitrypsin (alpha1 - protease inhibitor), causing an imbalance between elastolytic and antielastolytic factors, which leads to emphysema [6].
Estrogen deficiency promotes cigarette smoke–induced changes in the extracellular matrix in the lungs of aging female mice
2016, Translational ResearchCitation Excerpt :We also studied the coordinate regulation of apoptosis and estrogen status. Alveolar septal cell apoptosis and increased oxidant stress are known to contribute to the pathogenesis of emphysema.35,52,53 Apoptosis is primarily mediated by mitochondria, which are also the main source of free radicals.54
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