ReviewCurrent opinion in hematology2017
Ser/Thr protein kinase Bβ-NADPH oxidase 2 signaling in thromboinflammation.
Review in Current opinion in hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Adjunctive therapeutic strategy for in-stent thrombosis:RSC advances · 2026Article
- ERO1-PDI Redox Signaling in Health and Disease.Antioxidants & redox signaling · 2021Review
- Repurposing pyridoxamine for therapeutic intervention of intravascular cell-cell interactions in mouse models of sickle cell disease.Haematologica · 2020Article
- Protein disulfide isomerase in cardiovascular disease.Experimental & molecular medicine · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
purpose of reviewInteractions between neutrophils and platelets contribute to the progression of thromboinflammatory disease. However, the regulatory mechanism governing these interactions is poorly understood. The present review focuses on the crucial role of Ser/Thr protein kinase B (AKT)β-NADPH oxidase 2 (NOX2) signaling in regulating neutrophil and platelet activation and their heterotypic interactions under thromboinflammatory conditions. RECENT
findingsGrowing evidence has shown that platelets, leukocytes, and blood coagulation need to be considered to treat thromboinflammatory disease in which inflammation and thrombosis occur concurrently. In addition to plasma proteins and intracellular signaling molecules, extracellular reactive oxygen species (ROS) produced from activated leukocytes could be an important factor in the pathophysiology of thromboinflammatory disease. Recent studies reveal that AKT2-NOX2 signaling has critical roles in Ca mobilization, ROS generation, degranulation, and control of the ligand-binding function of cell surface molecules, thereby promoting heterotypic cell-cell interactions in thromboinflammation. These findings have provided novel insights into attractive therapeutic targets for the prevention and treatment of thromboinflammatory disease. SUMMARY: Recent discoveries concerning molecular mechanisms regulating neutrophil-platelet interactions have bridged some gaps in our knowledge of the complicated signaling pathways exacerbating thromboinflammatory conditions.
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