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25 cze 2022 · Based on recent studies, endosomal dependence can compensate for S protein priming to mediate SARS-CoV-2 infection of CMs, damage the contractile function of CMs, trigger electrical dysfunction, and tip the balance of the renin–angiotensin–aldosterone system to exert a myocardial injury effect.
10 paź 2022 · Clearance of the K287T virus from most infected cells by 7 dpi leads to a lower immune-mediated cytotoxicity, which correlates with lack of cardiac injury.
5 maj 2023 · Data point to pericytes as the primary target of SARS-CoV-2 in the heart. Infection of pericytes can account for the observed pericyte and endothelial cell death, innate immune response, and immunothrombosis commonly observed in COVID-19 hearts.
24 lut 2021 · There are several reasons to consider the role of endothelial cells in COVID-19 and other emerging viral infections. First, severe cases of COVID-19 show a common breakdown of central vascular functions. Second, SARS-CoV-2 replicates in endothelial cells.
28 paź 2021 · FIGURE 1. Cytoskeleton and mechanosensors play crucial roles during viral infections. (A) Actin filaments in host cells participate in virus surfing before entering into the cells. (B) Actin filaments provide forces for viral entry through clathrin-mediated endocytosis.
19 cze 2024 · Myocarditis is a secondary myocardium disease. Through histopathological tests, myocarditis is characterized by infiltration of immune cells, non-ischemic injury, and necrosis of cardiomyocytes.
1 lut 2022 · The current literature supports the notion that SARS-CoV-2 particles access the heart either by the circulating blood cells or by extracellular vesicles, originating from the inflamed lungs, and encapsulating the virus along with its receptor (ACE2).