The beneficial role of Hepcidin peptide inhibitor in improved the symptoms of COVID-19 in diabetics: anti-inflammatory and potential therapeutic effects

Abstract

Coronavirus Disease 2019 (COVID-19) is a recent public health issue worldwide. Also, diabetes is a frequent condition with high mortality. There is a strong relationship between COVID-19 and diabetes. This article analyses the intricate relationship between COVID-19 and hepcidin. Hepcidin increases in aged non-insulin diabetic patients. Hepcidin is the last target treatment of several medications commonly used. Viral diseases, especially SARS-CoV19, can activate the hepcidin pathway leading to an elevation in the iron load. This increased iron is released into the bloodstream and results in cell death through ferroptosis, like free iron. Excess iron has pro-coagulative and toxic effects. Hepcidin overexpression and iron overload are associated with COVID-19 infection and can be considered potential targets for treatment. Several studies have shown dalteparin (anti-Hepcidin) could improve the symptoms of COVID-19 in diabetics by appropriately modulating and decreasing oxidative stress and inflammation. This finding can be leading to enhancing the existing knowledge about Therapeutic measures for reducing Covid-19 impairments in diabetics and is suggested as a possible therapeutic agent in diabetes.

Links between Vitamin K, Ferroptosis and SARS-CoV-2 Infection

“…Host cells’ increased cellular metabolism and optimal iron levels are required for viral replication [ 85 ]. The hepcidin/ferroportin axis significantly regulates systematic iron [ 86 , 87 ]. Hepcidin, in a regular expression, has a protective function against infections.…”

“…The SARS-CoV-2 infection causes high levels of IFN-γ, interleukin 1-beta (IL1-β), interferon-inducible protein 10 (IP10), and monocyte chemotactic protein 1 (MCP1) [ 87 ]. Therefore, stimulation of these cytokines may cause hepcidin synthesis resulting in the accumulation of iron in macrophages [ 87 ]. Moreover, the infection leads to an inflammatory state in which IL-6 stimulates the synthesis of FER and hepcidin [ 91 , 92 ].…”

“…Iron converts the LOOH into hydroxyl radicals via the Fenton reaction, ultimately inducing ferroptosis and promoting cell damage [ 95 ]. Transferrin receptor-1 (TfR-1) can facilitate the entrance of iron held by transferrin into the cells [ 87 ]. TfR-1 is an ideal portal for the entry of various microorganisms into the cells [ 88 ].…”

“…TfR-1 is an ideal portal for the entry of various microorganisms into the cells [ 88 ]. It was observed that TfR-1 protein concentration in the lungs is significantly exalted in viral infection [ 87 ]. The virus can interact precisely with this receptor using its spike protein [ 94 ].…”

Clinical Significance of Serum Iron in the Diagnosis of Iron Deficiency Anemia in Patients from Local Population of Punjab-Lahore

“…Patients with thalassemia have been shown to have elevated levels of malondialdehyde and other plasma lipid peroxidation indicators . 25,26,27,28 According to a paper, unstable hemoglobin chains undergo auto-oxidation, which results in the production of H2O2 and superoxide 30,31 . Thus, in the presence of H2O2, this free nonheme iron can catalyze the Haber-Weiss reaction, producing a feral moiety and a hydroxyl radical.…”