| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T133 |
0-125 |
Sentence |
denotes |
Metabolic abnormalities, oxidative stress, chemokines, cytokines and by products of DAMPs cause endothelial cell injury [40]. |
| T134 |
126-270 |
Sentence |
denotes |
While the toxic effect(s) can be direct, impaired epi-genetic regulation and activation of resident neutrophils and macrophages also contribute. |
| T135 |
271-431 |
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 |
432-563 |
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 |
564-724 |
Sentence |
denotes |
Endothelial cells produce macrovesicles in response to inflammatory conditions and inflammatory mediators, including cytokines, thrombin and complement 5a [43]. |
| T138 |
725-841 |
Sentence |
denotes |
In turn, the endothelial cell macrovesicles impair adherans junctions, promote neutrophil binding and release NETs. |
