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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the pathogen responsible for the coronavirus disease 2019 (COVID-19), has been associated with the manifestation of adverse pulmonary conditions, such as pneumonia and acute respiratory distress syndrome (ARDS). A recent Nature Communications study identifies ferroptosis as a major cell death mechanism underlying COVID-19 lung disease . Study: Fatal COVID-19 pulmonary disease involves ferroptosis.

Image Credit: Mang E / Shutterstock.com Both acute and non-acute pulmonary damage have been associated with COVID-19. Severely infected COVID-19 patients often develop ARDS, which accounts for high mortality and poor prognosis.



Lung histology of patients with ARDS has indicated acute lung injury (ALI), particularly diffuse alveolar damage (DAD). The early stage of ARDS has been characterized by edema, hyaline membranes, and fibrosis. Non-acute lung injury (non-ALI) of COVID-19 patients includes microthrombi and pulmonary vascular congestion with hemangiomatosis-like changes.

COVID-19 pulmonary pathology has been associated with host inflammatory responses, including the cytokine storm and viral infection damage. Chronic immune responses induced by macrophages and neutrophils aggravate pulmonary tissue damage. Furthermore, immune cells lead to a release of reactive oxygen species and free radicals, thereby causing oxidative injury.

Although many supportive treatments, such as mechanical ventilation and intubation, are .

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