PMC:7373848 / 19011-20230 JSONTXT 11 Projects

Annnotations TAB TSV DIC JSON TextAE

Id Subject Object Predicate Lexical cue
T132 0-57 Sentence denotes Endothelial cells are a target for inflammatory mediators
T133 58-183 Sentence denotes Metabolic abnormalities, oxidative stress, chemokines, cytokines and by products of DAMPs cause endothelial cell injury [40].
T134 184-328 Sentence denotes While the toxic effect(s) can be direct, impaired epi-genetic regulation and activation of resident neutrophils and macrophages also contribute.
T135 329-489 Sentence denotes Products of vascular injury recruit neutrophils through several signaling pathways, including PI3K/AKt/eNOS/NF-Kβ and ERK1/2/P38 MAPK-activated protein kinases.
T136 490-621 Sentence denotes Recruited neutrophils subsets promote inflammation and further injury by releasing TNF-α, IL-1 and IL-8, and forming NETs [41, 42].
T137 622-782 Sentence denotes Endothelial cells produce macrovesicles in response to inflammatory conditions and inflammatory mediators, including cytokines, thrombin and complement 5a [43].
T138 783-899 Sentence denotes In turn, the endothelial cell  macrovesicles impair adherans junctions, promote neutrophil binding and release NETs.
T139 900-1219 Sentence denotes Released during periods of cell death and immune activation, histone, nucleosomes and NETs induce cytotoxicity by altering cell membrane permeability to calcium ions, activating TLRs on innate immune cells, stimulating NLRP3 inflammasome and complement systems, resulting in a sterile pro-inflammatory environment [44].