Pulmonary emphysema is a chronic lung condition in which the alveoli are destroyed, narrowed, collapsed, stretched, or over-inflated. Over-inflation of the air-sacs is a result of a breakdown of the walls of the alveoli, and causes a decrease in respiratory function and breathlessness. Damage to the air sacs is irreversible and results in permanent "holes" in the tissues of the lower lungs.
This article talks apoptosis and it's role in pulmonary emphysema. Pulmonary emphysema is a powerful phenomenon that involves the gradual destruction of extracellular matrix by presence of an extra amount of proteases, but also apoptosis, cellproliferation, and senescence (process of deterioration with age). Cellular proliferation makes up for enhanced alveolar cell death, whereas cell aging caused by cigarette smoking and increased cell turnover slows/stops cell proliferation, leading to apoptosis. As a result, alveolar cells gradually disappear and emphysematous lesions advance. At the same time, cellular senescence causes long-term inflammation through enhanced production of proinflammatory cytokines. Recent research suggests that DNA damage (double strand breaks) underlies the molecular mechanisms of these factors in the gradual destruction of extracellular matrix; apoptosis, cell senescence, and chronic inflammation.
This picture shows the difference between normal alveoli and alveoli with pulmonary emphysema.
This article talks apoptosis and it's role in pulmonary emphysema. Pulmonary emphysema is a powerful phenomenon that involves the gradual destruction of extracellular matrix by presence of an extra amount of proteases, but also apoptosis, cellproliferation, and senescence (process of deterioration with age). Cellular proliferation makes up for enhanced alveolar cell death, whereas cell aging caused by cigarette smoking and increased cell turnover slows/stops cell proliferation, leading to apoptosis. As a result, alveolar cells gradually disappear and emphysematous lesions advance. At the same time, cellular senescence causes long-term inflammation through enhanced production of proinflammatory cytokines. Recent research suggests that DNA damage (double strand breaks) underlies the molecular mechanisms of these factors in the gradual destruction of extracellular matrix; apoptosis, cell senescence, and chronic inflammation.
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