Intracellular organelles remodeling in myocardial endotheliocytes in COVID-19: an autopsy-based study

It is known that the unfavorable outcome in patients infected with SARS-CoV-2 may be associated with the development of complications caused by heart damage due to the direct virus action. The mechanism of these cardiovascular injuries caused by SARS-CoV-2 infection has not been fully understood; however, the study of COVID-19-associated myocardial microcirculatory dysfunction can represent the useful strategy to solving this challenge. Thus, here we aimed to study the ultrastructural organization of endothelial cells of myocardial capillaries in patients with COVID-19. The morphology of endotheliocytes of the myocardial blood capillaries in patients with COVID-19 was studied on cardiac autopsy material using transmission electron microscopy. The endotheliocytes of myocardial capillaries in patients with COVID-19 were characterized by the abundant rough endoplasmic reticulum (ER) membranes, the Golgi complex, and free polysomal complexes of ribosomes and lipids. The presence of double membrane vesicles with virions and zippered ER was detected in the cytoplasm of endotheliocytes. The revealed endothelial ultrastructural changes indicate the remodeling of intracellular membranes during SARS-CoV-2 infection. Our findings confirm the formation of virus-induced structures in myocardial endothelial cells considered critical for viral replication and assembly. The data may elucidate the mechanisms of endothelial dysfunction development in patients with COVID-19 to provide potential targets for drug therapy.

Automated summary

This study examined the ultrastructural organization of endothelial cells in myocardial capillaries of COVID-19 patients. Electron microscopy revealed the presence of abundant rough endoplasmic reticulum, Golgi complex, and vesicles with virions and zippered endoplasmic reticulum in the endothelial cells. These findings suggest that COVID-19 can lead to remodeling of intracellular membranes and the formation of virus-induced structures critical for viral replication and assembly in myocardial endothelial cells. The data could provide insights into the development of endothelial dysfunction in COVID-19 patients and potential targets for drug therapy.