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Activated caspase-8 subsequently triggers pro-apoptotic caspases-9, -7, and -3, while downregulating anti-apoptotic proteins Bcl-xL and Bcl-2, thereby promoting apoptosis

15 Collectively, these events lead to a vicious cycle of persistent inflammation and chronic oxidative stress, which results in protease-anti-protease imbalance, defects in tissue repair mechanisms, accelerated apoptosis in lung cells and progression of COPD