Abstract
Abstract The growing rate of COVID-19 infection has resulted in serious health crisis and caused a huge socio-economic burden across the globe. Apart from the respiratory system, COVID-19 displayed severe pathological impact on other organs especially in the cardiovascular system as evident from the increased risk of infection and mortality among CVD patients. Information on the underlying molecular mechanisms associated with the aggravated CVD pathology in COVID-19 patients are largely unknown. Here, we provide an insight into the possible molecular target(s) to intervene the effects of COVID-19-induced exacerbations and complications in CVD patients. Inspired from the knowledge on SARS-CoV virology and its closeness to COVID-19, we present potential molecular associations focusing on central ACE2 signaling axis and interconnecting the major sheddases (ADAM 17 and CTSL), TLRs, and NLRP3 inflammasome as the major transit points contributing to overall pro-inflammatory pool and subsequent cytokine burst leading to aggravated COVID-19-CVD comorbidity. Further understanding of these molecular mysteries in ideal in-vitro and in-vivo models would open novel translational avenues for effective management of COVID-19-CVD comorbidity.
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