COVID-19 is characterized by a highly (pro)thrombotic state in patients infected with coronavirus SARS-CoV-2. It is known that the host inflammatory and immunity response and inflammatory and prothrombotic properties of the pathogen itself, the coronavirus, all contribute to thrombotic events in COVID. Eventually, vascular damage will result in Multiple Organ Failure (MOF) and loss of function, rendering "recovered" or patients who had "mild symptoms" with long-term COVID complications.
Of the many mechanisms involved in thrombosis caused by SARS-CoV-2 infection, the Complement System, the Renin-Angiotensin-Aldosterone (RAS/RAAS) and Kallikrein-Kinin System (KKS), have a key role in mediating thrombotic events. In the next slides, I will show you therapeutic options to treat COVID-19 along the lines of the Complement, RAS, thromboinflammatory and Central Nervous System pathways:
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