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It is accompanied by a series of interwoven pathological features, including airway/lung parenchymal cell damage and death, structural remodeling, and immune dysfunction ( In the aforementioned pathological axis, the abnormal activation and imbalance of cell death programs are important hubs connecting barrier destruction, inflammation amplification, and tissue remodeling ( + T cell exhaustion and autoimmune-like responses, thus forming a critical bridge between innate immune activation and adaptive immune dysfunction ( However, it is important to emphasize that COPD is not driven by a single type of PCD. On the contrary, COPD is more consistent with a dynamic, context-dependent PCD landscape: different cell types (airway epithelium, alveolar epithelium, endothelium, and immune cells) initiate different death programs under different stimuli (tobacco smoke, pathogens, particulate matter, persistent oxidative stress, and DAMPs, etc.)
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A retrospective longitudinal multicenter cohort study indicated that patients with COVID-19-related AKI were generally younger, had a higher baseline eGFR, worse baseline comorbidity scores, elevated markers of illness severity, and longer hospital stay compared to those suffering from influenza-related AKI or other types of AKI [49]
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