We are analyzing https://link.springer.com/article/10.1007/s11239-025-03101-6.

Title:
Advancements in research on the thrombo-inflammation mechanisms mediated by factor XII in ischemic stroke | Journal of Thrombosis and Thrombolysis
Description:
Ischemic stroke (IS) is a major cause of mortality and disability, with thrombo-inflammation constituting a core pathophysiological mechanism. This process is closely linked to coagulation cascade activation, endothelial injury, immune cell infiltration, and neuronal damage. Coagulation factor XII (FXII), a key mediator of the contact activation pathway, has emerged as a promising therapeutic target due to its dual role in pathological thrombosis and immune regulation, without compromising physiological hemostasis. However, the clinical translation of FXII-targeted therapies is hindered by paradoxical observations. Recent studies highlight that FXII’s functional complexity stems from its structural and spatial heterogeneity: full-length FXII derived from the liver and short FXII mRNA isoforms expressed in neurons mediate distinct biological effects. While FXII contributes to neuroinflammation and vascular injury via endothelial-platelet-neutrophil interactions, neuron-derived FXII exhibits neuroprotective effects through HGF-mediated signaling pathways. Additionally, circulating FXIIa promotes vascular remodeling by enhancing endothelial growth factor (VEGF) release. This review summarizes the multifaceted regulatory mechanisms of FXII in IS, focusing on its structure, distribution, preclinical-clinical paradox, and current therapeutic strategies. Special emphasis is placed on its domain-specific functions and the neuroprotective effects of FXII. Graphical Abstract
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28 years and 1 months (reg. 1997-05-29).

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pubmed, article, google, scholar, cas, factor, central, xii, stroke, wang, coagulation, ischemic, blood, brain, renné, injury, thromb, httpsdoiorgs, thrombosis, liu, activation, chen, zhang, gailani, mice, thromboinflammation, cell, inflammation, httpsdoiorgblood, haemost, xiia, hunan, research, yang, fxii, kleinschnitz, cerebral, sci, human, cells, microglia, medicine, immune, pathway, promotes, review, access, front, nat, chinese,

Topics {✒️}

inhibiting ros/nlrp3-mediated pyroptosis stat1/stat6/pparγ signaling pathways ros-dependent net formation month download article/chapter single-chain factor xii monocyte-related cytokines/chemokines monocyte-derived macrophages contribute mitogen-activated protein kinase anti-factor xii autoantibodies factor xii-induced mitogenesis factor xii/xiia inhibitors hgf-mediated signaling pathways integrin-mediated neutrophil adhesion cerebral ischemia/reperfusion injury thrombo-inflammation mechanisms mediated b2 receptor-mediated signaling liver-derived factor xii factor xiia inhibitor single-cell rna sequencing microglia-mediated immune inflammation kallikrein-kinin system endothelial-platelet-neutrophil interactions full-length fxii derived modulating m1/m2 polarization blood-brain barrier disruption blood-brain barrier permeability tumor necrosis factor-alpha cerebral ischemia/reperfusion rats year-long immune profile triazole-based potent inhibitors full article pdf human factor xiia de meyer sf neutrophil extracellular traps jak2/stat3 pathway factor xii dependent neutralizing blood-borne polyphosphate coagulation factor xii factor xii promotes activated hageman factor human neutrophil membrane thrombo-inflammation constituting factor xiia regulates induce inflammatory responses coagulation cascade activation neutrophils extracellular traps kinin-forming systems contact activation pathway anti-inflammatory activities epidermal growth factor

Questions {❓}

Kehrel BE, Fender AC (2016) Resolving thromboinflammation in the brain after ischemic stroke?

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      description:Ischemic stroke (IS) is a major cause of mortality and disability, with thrombo-inflammation constituting a core pathophysiological mechanism. This process is closely linked to coagulation cascade activation, endothelial injury, immune cell infiltration, and neuronal damage. Coagulation factor XII (FXII), a key mediator of the contact activation pathway, has emerged as a promising therapeutic target due to its dual role in pathological thrombosis and immune regulation, without compromising physiological hemostasis. However, the clinical translation of FXII-targeted therapies is hindered by paradoxical observations. Recent studies highlight that FXII’s functional complexity stems from its structural and spatial heterogeneity: full-length FXII derived from the liver and short FXII mRNA isoforms expressed in neurons mediate distinct biological effects. While FXII contributes to neuroinflammation and vascular injury via endothelial-platelet-neutrophil interactions, neuron-derived FXII exhibits neuroprotective effects through HGF-mediated signaling pathways. Additionally, circulating FXIIa promotes vascular remodeling by enhancing endothelial growth factor (VEGF) release. This review summarizes the multifaceted regulatory mechanisms of FXII in IS, focusing on its structure, distribution, preclinical-clinical paradox, and current therapeutic strategies. Special emphasis is placed on its domain-specific functions and the neuroprotective effects of FXII.
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