About the Special Issue

Stroke remains one of the most devastating and challenging neurological diseases worldwide. Inflammation, as well as oxidative stress is one of the main contributors to post-stroke injuries, and oxidative stress can further induce inflammation. Moreover, the inflammatory response is closely related to immune modulation in ischemic stroke progression. Hence, major ischemic stroke treatment strategies include targeting inflammatory responses, immune modulation (especially immune cells), and inflammatory response to suppress stroke progression. Signaling pathways are critical processes for immune cell activation and function in response to infections or diseases in acute ischemic stroke. For example, the TLR4/NF-κB and JAK/STAT pathways participate in the cerebral ischemic response. TLR4/NF-κB is one of the major signaling pathways regulating inflammation and apoptosis after ischemic insults. This pathway is activated in immune cells, such as peripheral monocyte/macrophage, leukocyte T cells, as well as vascular endothelial cells in the brain, and microglia. Once activated, NF-κB trans-locates to the nuclei and induces the expression of a series of genes, such as iNOS, COX-2, ICAM-1, Nox-2, cytokines, and chemokines, which enhances the recruitment of peripheral immune cells to the lesion site. Furthermore isturbance in primary hemostasis may contribute to a prothrombotic state leading to ischemic stroke. β-TG, beta-thromboglobulin; ADAMTS-13, a disintegrin and metalloprotease with trompospondin motif repeats 13; eDNA, extracellular DNA; GPVI, glycoprotein VI; NET, neutrophil extracellular trap; PAI-1, plasminogen activator inhibitor-1; TAFI, thrombin-activatable fibrinolysis inhibitor; TNF-α, tumor necrosis factor alpha; TPA, tissue-type plasminogen activator. Secondary hemostasis consists of the extrinsic and intrinsic pathways (the contact pathway of coagulation). Both pathways result in common pathway activation and formation of the fibrin clot. Several of these coagulation factors have been linked to Iischemic stroke.

Factor VIII (FVIII) functions as a cofactor for factor IXa that cleaves inactive FX into its activated form (FXa). Increased FVIII levels are a common risk factor for venous thrombosis and may also be associated with risk of stroke.

In this special issue the invited authors will summarize the role of inflammation in the pathogenesis of ischemic stroke and the involvement of the main coagulative factors involved in estrinsic and intrinsic mechanisms of the coagulation in brain ischemic damage.

Keywords: ischemic stroke; inflammation; coagulation; hemostasis; thrombosis

Call for Papers