Liver injury in COVID-19: Holds ferritinophagy-mediated ferroptosis accountable

Abstract

Even in patients without a history of liver disease, liver injury caused by coronavirus disease 2019 (COVID-19) is gradually becoming more common. However, the precise pathophysiological mechanisms behind COVID-19's liver pathogenicity are still not fully understood. We hypothesize that inflammation may become worse by cytokine storms caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Elevated ferritin levels can initiate ferritinophagy mediated by nuclear receptor coactivator 4 (NCOA4), which leads to iron elevation, and ferroptosis. In COVID-19 patients, ferroptosis can be restricted to reduce disease severity and liver damage by targeting NCOA4-mediated ferritinophagy. To confirm the role of ferritinophagy-mediated ferroptosis in SARS-CoV-2 infection, further research is required.

COVID-19 related neurological manifestations in Parkinson’s disease: has ferroptosis been a suspect?

“…Iron metabolism impairment, a significant contributor to PD [ 91 , 92 ], has been extensively established in a significant fraction of COVID-19 patients in response to SARS-CoV-2 infection [ 93 – 95 ], which corresponds with the risk of severe and fatal COVID-19 illness. In our previous study, we elaborated the mechanism of dysregulation of iron metabolism and ferritinophagy in COVID-19 [ 96 , 97 ]. In addition, ceruloplasmin levels in long-term COVID-19 patients exhibit a declining tendency when compared to those in COVID-19 patients and healthy controls [ 98 ].…”