Genetic Engineering and Biotech News
Over the past few years, researchers have uncovered countless details about how SARS-CoV-2 causes COVID-19. However, the mechanisms underlying how SARS-CoV-2 infection causes severe pulmonary manifestations remain poorly understood. This, in turn, limits treatment options.
In some severe cases of COVID-19, the lungs undergo extreme damage, resulting in a range of life-threatening conditions like pneumonia, inflammation, and acute respiratory distress syndrome. The root cause of those wide-ranging reactions in the lungs has remained unclear. However, hyperferritinemia and disrupted lung iron homeostasis in COVID-19 patients have pointed to ferroptosis—an iron-dependent cell death. Now, a new study finds that ferroptosis is the major cell death mechanism that underlies COVID-19 lung disease. In a new paper, the authors noted that “immunostaining and lipidomic analysis in COVID-19 lung autopsies reveal increases in ferroptosis markers, including transferrin receptor 1 and malondialdehyde accumulation in fatal cases.” The finding indicates that deliberately halting ferroptosis with therapeutic drug candidates could improve COVID-19 outcomes.