2016
DOI: 10.1016/j.carpath.2015.09.006
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Endogenous C1-inhibitor production and expression in the heart after acute myocardial infarction

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Cited by 12 publications
(9 citation statements)
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“…We found that EV-SerpinG1 in the TEX fraction was associated with higher odds of HF, which points to an increased inflammatory state in these patients. Serpin G1 TEX levels in the HF patient group differ between HF patients with and without MI which is in accordance with the association of SerpinG1 with ischemia [ 49 , 50 ].…”
Section: Discussionsupporting
confidence: 76%
“…We found that EV-SerpinG1 in the TEX fraction was associated with higher odds of HF, which points to an increased inflammatory state in these patients. Serpin G1 TEX levels in the HF patient group differ between HF patients with and without MI which is in accordance with the association of SerpinG1 with ischemia [ 49 , 50 ].…”
Section: Discussionsupporting
confidence: 76%
“…30 Among the altered complement -related factors in the present study, SERPING1, a member of a serine proteinase inhibitor (SERPIN) family, is a C1 inhibitor that regulates both complement activation and blood coagulation. 31,32 Consistent with our findings, Emmens et al 33 found that endogenous SERPING1 likely plays an important role in the regulation of complement activity following acute myocardial infarction, indicating that SERPING1 might be a novel biomarker and therapeutic target in ischemic heart disease. In summary, quantitative proteomic analysis identified differential protein expression in the left ventricle that can distinguish between patients with ICM and healthy individuals.…”
Section: Bioinformatics Analysis Of the Identified Pro-supporting
confidence: 90%
“…Interestingly the complement regulator C1 inhibitor was found to colocalize intracellularly in cardiomyoblasts and endothelial cells with the activation fragments C4d and C3d in a rat model of myocardial infarction (Emmens et al, 2016). Furthermore, the complement regulators FH and FI are also present in the cytoplasm of endothelial cells and the authors observed that these proteins are not secreted upon treatment with histamine, which usually induces the 'spillage' of innate effector molecules (Turner et al, 2015).…”
Section: The Complosome In Non-immune Cellsmentioning
confidence: 97%