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Neutrophil Extracellular Traps in Coronavirus Disease-19-Associated Ischemic Stroke: A Novel Avenue in Neuroscience

Tjokorda Istri Pramitasuri, Anak Agung Ayu Putri Laksmidewi, Ida Bagus Kusuma Putra, Felix Adrian Dalimartha

2021Experimental Neurobiology25 citationsDOIOpen Access PDF

Abstract

Ischemic stroke is one of the catastrophic neurological events that are being increasingly recognized among Coronavirus Disease (COVID)-19 patients. The recent studies have revealed about a possible connection among COVID-19, ischemic stroke, and excessive Neutrophil Extracellular Traps (NETs) formation. This paper establishes an overview of coronaviruses and NETs, NETs in pathogenesis of COVID-19 induced-ischemic stroke, and future directions using related recent literatures. NETs are normally functioned for a defense against pathogens, but in immoderate amount, they can trigger series of destructive events. Vasculopathy and neuroinflammation are the pathological mechanisms of NETs suggested to link COVID-19 and ischemic stroke. Based on newly discovered possible mechanisms, the potential clinical implications that could be applied consists of inhibition of NET formation, disrupting cholesterol synthesis, and interfering inflammatory pathway. A considerable number of scientific works are needed in order to complete the current understanding of the emerging relationship among COVID-19, NETs, and ischemic stroke. Although the exact mechanism is still unknown, these novel findings are a worthwhile contribution in defining future studies, suitable future frameworks, and therapeutic strategies.

Topics & Concepts

Neutrophil extracellular trapsNeuroscienceCoronavirus disease 2019 (COVID-19)CoronavirusStroke (engine)MedicineExtracellularSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2)Disease2019-20 coronavirus outbreakVirologyPsychologyPathologyBiologyInfectious disease (medical specialty)ImmunologyInflammationCell biologyOutbreakPhysicsThermodynamicsNeutrophil, Myeloperoxidase and Oxidative MechanismsNeuroinflammation and Neurodegeneration MechanismsS100 Proteins and Annexins
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