SARS-CoV-2 infection promotes vascular smooth muscle cell proliferation and vascular calcification through pathways involving cholesterol, calcium, and phosphate, worsening COVID-19 prognosis.
SARS-CoV-2 may worsen cardiovascular prognosis in COVID-19 patients by inducing a phenotypic switch in vascular smooth muscle cells via cholesterol, calcium, and phosphate pathways, leading to vascular calcification.
Although the novel coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), primarily manifests as severe respiratory distress, its impact on the cardiovascular system is also notable. Studies reveal that COVID-19 patients often suffer from certain vascular diseases, partly attributed to increased proliferation or altered phenotype of vascular smooth muscle cells (VSMCs). Although the association between COVID-19 and VSMCs is recognized, the precise mechanism underlying SARS-CoV-2's influence on VSMC phenotype remains largely under-reviewed. In this context, while there is a consistent body of literature dissecting the effect of COVID-19 on the cardiovascular system, few reports delve into the potential role of VSMC switching in the pathophysiology associated with COVID-19 and the molecular mechanisms involved therein. This review dissects and critiques the link between COVID-19 and VSMCs, with particular attention to pathways involving cholesterol, calcium, and phosphate. These pathways underpin the interaction between the virus and VSMCs. Such interaction promotes VSMC proliferation, and eventually potentiates vascular calcification as well as worsens prognosis in patients with COVID-19.
Ghanem et al. (Mon,) conducted a review in COVID-19. SARS-CoV-2 infection was evaluated on Vascular smooth muscle cell phenotypic switch and proliferation. SARS-CoV-2 infection promotes vascular smooth muscle cell proliferation and vascular calcification through pathways involving cholesterol, calcium, and phosphate, worsening COVID-19 prognosis.