Alteration of Iron homeostatis in Ferroptosis biomarkers among COVID-19 patients: A Review Article

Abstract

The first case of a patient infected by the SARS-CoV-2, causing viral pneumonia, which was presented in December 2019 in the city of Wuhan/ China (Guan et al., 2020). According to the World Health Organization, SARS-CoV-2 infection reached pandemic status on 20 January 2020 (Mahase, 2020). The disease caused by SARS-CoV-2 is named Coronavirus Diseases-2019 (COVID-19). Genome comparisons have shown that previous isolates, the SARS-related coronavirus (SARSr-CoV), including the SARS-CoV are closely related, yet different in disease manifestation (Low et al., 2021). Which is considered similar to SARS-CoV, invades human cells via the receptor angiotensin converting enzyme II (ACE2), lung cells that have ACE2 expression may be the main target cells during SARS-CoV-2 infection. Some patients also exhibit non-respiratory symptoms, such as kidney failure, implying that SARS-CoV-2 could also invade other organs(Zou et al., 2020), so, lung is not the only organ affected by SARS-CoV-2; the virus can affect various systems and result in multiple organ failure (Zaim et al., 2020). A recent reported case of SARS-CoV-2 myocarditis with cardiogenic shock showed a signature of myocardial and kidney ferroptosis, a novel, iron-dependent programmed cell death(Pasini et al., 2021). Ferroptosis is a relatively novel cell death type that was first termed by Dixon et al. in 2012, ferroptosis is an iron-dependent regulated cell death (RCD) characterized by iron overload and lipid peroxidation. The main morphological features of ferroptosis are mitochondrial shrinkage accompanied by increased mitochondrial membrane density and degenerated mitochondrial crista without changes in the nucleus(Dixon et al., 2012).