Acute COVID-19, Long COVID, Post COVID-vaccination syndrome & Cardiovascular System-Experimental Studies

This study is the first to show that the SARS-CoV-2 spike protein activates β-adrenergic receptors in cardiomyocytes, contributes to cardiac sympathetic hyperactivity and increases activation of downstream β-adrenergic receptor signaling induced by epinephrine.

The S1 protein activates human CFs by priming NLRP3 inflammasomes through NF-κB signaling in an ACE2-dependent way.

This study showed for the first time that mRNA-1273 and BNT162b2 COVID-19 vaccines induced cardiotoxic effects with disturbances of normal contractile function in rat cardiomyocytes. The effects of vaccines differed fundamentally in their pathophysiological mechanisms.

Human iPS cell-based cardiac tissue model shows that cardiac tissue exposed to persistent SARS-CoV-2 infection is at high risk for cardiac dysfunction.