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作 者:Panagiota Gianni Mark Goldin Sam Ngu Stefanos Zafeiropoulos Georgios Geropoulos Dimitrios Giannis
机构地区:[1]Department of Internal Medicine III,Hematology,Oncology,Palliative Medicine,Rheumatology and Infectious Diseases,University Hospital Ulm,Ulm 89070,Germany [2]School of Medicine at Hofstra/Northwell,Northwell Health,New York,NY 11549,United States [3]Feinstein Institutes for Medical Research at Northwell Health,Feinstein Institutes,New York,NY 11030,United States [4]Elmezzi Graduate School of Molecular Medicine,Northwell Health,New York,NY 11030,United States [5]Department of General Surgery,University College London Hospitals,London NW12BU,United Kingdom [6]North Shore/Long Island Jewish General Surgery,Northwell Health,New York,NY 11021,United States
出 处:《World Journal of Experimental Medicine》2022年第4期53-67,共15页世界实验医学杂志
摘 要:Coronavirus disease 2019(COVID-19)causes acute microvascular thrombosis in both venous and arterial structures which is highly associated with increased mortality.The mechanisms leading to thromboembolism are still under investigation.Current evidence suggests that excessive complement activation with severe amplification of the inflammatory response(cytokine storm)hastens disease progression and initiates complement-dependent cytotoxic tissue damage with resultant prothrombotic complications.The concept of thromboinflammation,involving overt inflammation and activation of the coagulation cascade causing thrombotic microangiopathy and end-organ damage,has emerged as one of the core components of COVID-19 pathogenesis.The complement system is a major mediator of the innate immune response and inflammation and thus an appealing treatment target.In this review,we discuss the role of complement in the development of thrombotic microangiopathy and summarize the current data on complement inhibitors as COVID-19 therapeutics.
关 键 词:COVID-19 COMPLEMENT Microvascular injury THROMBOEMBOLISM Cytokine storm Thrombotic microangiopathy
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