For years, arrhythmias have been well documented in the medical arena as a cardiovascular consequence of iron overload (IO). They are thought to be linked to the accumulation of iron in the myocardium. Iron is the earth's fourth most abundant element and the second most plentiful metal (after aluminium). When it comes to biology, iron fills two roles: it's necessary and it's poisonous. It is necessary as a trace iron element since it is found in hemoproteins such as haemo-globin, but it is poisonous in excess amounts of the ability to produce free radicals, which can harm the biological system. The high prevalence of cardiomyopathy in patients with hemosiderosis, particularly in cases of transfusional iron overload, strongly suggests that iron deposition in the heart plays a key role in the development of heart failure. Thalassemia major, which necessitates blood transfusion as a treatment, absorbs a large amount of iron in the patient's duodenum. Moreover, Iron Overload causes a threat to vital organs such as the liver and, initiates events of the pathologic progression involving apoptosis, fibrosis, and ultimately cardiac dysfunction. Furthermore, we discuss the iron overload issue as it relates to beta-thalassemia major patient blood transfusion treatment, as well as key individuals accountable for iron excess that ultimately leads to cardiomyopathy.

The ongoing pandemic that resulted from coronavirus disease (COVID-19), which is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), had been spiraling out of control with no known antiviral drugs or vaccines. Due to the extremely serious nature of the disease, it has claimed many lives, with a mortality rate of 3.4% declared by the World Health Organization (WHO) on March 3, 2020. The aim of this study is to gain an understanding of the regulatory nature of the proteins involved in COVID-19 and to explore the possibility that microRNA (miRNA) could become a major component in the decoding of the virus. In the study, we were able to correlate the host protein gene BCL2L1 with miRNA miR-23b via network analysis. MiRNAs have previously been associated with the antiviral properties of various viral diseases, such as enterovirus 71 and hepatitis. They have been reported to act as antiviral regulators, since they are an integral component in the direct regulation of viral genes. MiRNAs are also capable of enabling the virus to avoid the host immune response by suppressing the IFN-α/β signaling pathway or increasing the production of IFN-α/β and as a result, inhibiting the viral infection. Here, we explain and shed light on the various correlations in the miRNA-gene-disease association that are seen in the host proteins of COVID-19.