2020
DOI: 10.1098/rsob.200161
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Endothelial cells, neutrophils and platelets: getting to the bottom of an inflammatory triangle

Abstract: Severe fibrotic and thrombotic events permeate the healthcare system, causing suffering for millions of patients with inflammatory disorders. As late-state consequences of chronic inflammation, fibrosis and thrombosis are the culmination of pathological interactions of activated endothelium, neutrophils and platelets after vessel injury. Coupling of these three cell types ensures a pro-coagulant, cytokine-rich environment that promotes the capture, activation and proliferation of circulating immune cells and r… Show more

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Cited by 34 publications
(22 citation statements)
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References 207 publications
(323 reference statements)
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“…Our study did not show a correlation of serum SDC1 with catecholamines or blood pressure, suggesting that eGC damage is likely not responsible for the elevated serum SDC4 in the women who displayed the higher levels of blood pressure. This is further corroborated by the fact that there was no correlation between SDC4 and circulating pro-inflammatory cytokines, which are an end product of damaged glycocalyx [38].…”
Section: Discussionmentioning
confidence: 71%
“…Our study did not show a correlation of serum SDC1 with catecholamines or blood pressure, suggesting that eGC damage is likely not responsible for the elevated serum SDC4 in the women who displayed the higher levels of blood pressure. This is further corroborated by the fact that there was no correlation between SDC4 and circulating pro-inflammatory cytokines, which are an end product of damaged glycocalyx [38].…”
Section: Discussionmentioning
confidence: 71%
“…Thrombosis, chronic inflammation, and fibrosis are at the end of the pathological interactions of activated endothelium, neutrophils, and platelets [100]. Either pure or food-derived polyphenols have been reported to decrease endothelial dysfunction and endothelial cell activation in vitro, ex vivo, and in animal models of endothelial dysfunction by decreasing oxidant production.…”
Section: Shear Stress-induced Platelet Aggregationmentioning
confidence: 99%
“…HNE induces endothelial cell insulin resistance, and the associated akt inhibition both inhibits eNOS and upregulates the vasoconstrictor, endothelin [3,53]. The dysfunctional endothelial cells further produce pro-inflammatory factors such as TNFα, IL-1ÎČ, IL-8 and MCP-1 which recruit circulating neutrophils, platelets and monocytes, and the latter differentiate into macrophages [53,54]. Neutrophils, monocytes and macrophages secrete myeloperoxidase [55].…”
Section: Hypertensionmentioning
confidence: 99%