This article was originally published here
J Cardiovasc Pharmacol. 2021 Dec 10. doi: 10.1097/FJC.0000000000001201. Online ahead of print.
ABSTRACT
The ongoing COVID-19 pandemic caused by SARS-CoV-2 has significant implications for patients with concomitant cardiovascular disease (CVD), as they are the population at the greatest risk of death. The treatment of such patients and complications may represent a new challenge for the fields of cardiology and pharmacology. Thus, understanding the involvement of this viral infection in CVD might help to reduce the SARS-CoV-2 multiorgan potential of aggressiveness. SARS-CoV-2 disturbs the host epigenome and several epigenetic processes involved in the pathophysiology of COVID-19 that can directly affect the function and structure of the cardiovascular system (CVS). Hence, it would be relevant to identify epigenetic alterations that directly impact CVS physiology after SARS-CoV-2 infection. This could contribute to the view of this virus-induced CVS injury and direct forthcoming tackles for COVID-19 treatment to reduce mortality in patients with CVD. Targeting epigenetic marks could offer strong evidence for the development of novel antiviral therapies, especially in the context of COVID-19-related CVS damage. In this review, we address some of the main signaling pathways which are currently known as being involved in COVID-19 pathophysiology and the importance of this glint on epigenetics and some of its modifiers (epidrugs) to control the unregulated epitope activity in the context of SARS-CoV-2 infection, COVID-19, and underlying CVD.
PMID:34935698 | DOI:10.1097/FJC.0000000000001201
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