FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2891941122> ?p ?o ?g. }

• W2891941122 abstract "Human ascending aortic aneurysms characteristically exhibit cystic medial degeneration of the aortic wall encompassing elastin degeneration, proteoglycan accumulation smooth muscle cell loss. Most studies have focused on the aortic media and there is a limited understanding of the importance of the adventitial layer in the setting of human aneurysmal disease. We recently demonstrated that the adventitial ECM contains key angiogenic factors that are downregulated in aneurysmal aortic specimens. In this study, we investigated the adventitial microvascular network (vasa vasorum) of aneurysmal aortic specimens of different etiology and hypothesized that the vasa vasorum is disrupted in patients with ascending aortic aneurysm. Morphometric analyses of hematoxylin and eosin-stained human aortic cross-sections revealed evidence of vasa vasorum remodeling in aneurysmal specimens, including reduced density of vessels, increased lumen area and thickening of smooth muscle actin-positive layers. These alterations were inconsistently observed in specimens of bicuspid aortic valve (BAV)-associated aortopathy, while vasa vasorum remodeling was typically observed in aneurysms arising in patients with the morphologically normal tricuspid aortic valve (TAV). Gene expression of hypoxia-inducible factor 1α and its downstream targets, metallothionein 1A and the pro-angiogenic factor vascular endothelial growth factor, were down-regulated in the adventitia of aneurysmal specimens when compared with non-aneurysmal specimens, while the level of the anti-angiogenic factor thrombospondin-1 was elevated. Immunodetection of glucose transporter 1 (GLUT1), a marker of chronic tissue hypoxia, was minimal in non-aneurysmal medial specimens, and locally accumulated within regions of elastin degeneration, particularly in TAV-associated aneurysms. Quantification of GLUT1 revealed elevated levels in the aortic media of TAV-associated aneurysms when compared to non-aneurysmal counterparts. We detected evidence of chronic inflammation as infiltration of lymphoplasmacytic cells in aneurysmal specimens, with a higher prevalence of lymphoplasmacytic infiltrates in aneurysmal specimens from patients with TAV compared to that of patients with BAV. These data highlight differences in vasa vasorum remodeling and associated medial chronic hypoxia markers between aneurysms of different etiology. These aberrations could contribute to malnourishment of the aortic media and could conceivably participate in the pathogenesis of thoracic aortic aneurysm." @default.
• W2891941122 created "2018-09-27" @default.
• W2891941122 creator A5000015310 @default.
• W2891941122 creator A5027652711 @default.
• W2891941122 creator A5031145615 @default.
• W2891941122 creator A5060547232 @default.
• W2891941122 creator A5088386918 @default.
• W2891941122 date "2018-09-17" @default.
• W2891941122 modified "2023-10-13" @default.
• W2891941122 title "Medial Hypoxia and Adventitial Vasa Vasorum Remodeling in Human Ascending Aortic Aneurysm" @default.
• W2891941122 cites W1434966346 @default.
• W2891941122 cites W1455607059 @default.
• W2891941122 cites W1503573748 @default.
• W2891941122 cites W1525416908 @default.
• W2891941122 cites W1929366836 @default.
• W2891941122 cites W1965543940 @default.
• W2891941122 cites W1973749498 @default.
• W2891941122 cites W1974961631 @default.
• W2891941122 cites W1987060644 @default.
• W2891941122 cites W1988100039 @default.
• W2891941122 cites W1993170727 @default.
• W2891941122 cites W2004436993 @default.
• W2891941122 cites W2004815773 @default.
• W2891941122 cites W2012517517 @default.
• W2891941122 cites W2017574292 @default.
• W2891941122 cites W2023229209 @default.
• W2891941122 cites W2033486658 @default.
• W2891941122 cites W2034930271 @default.
• W2891941122 cites W2038136158 @default.
• W2891941122 cites W2040749098 @default.
• W2891941122 cites W2043255601 @default.
• W2891941122 cites W2048672117 @default.
• W2891941122 cites W2049175174 @default.
• W2891941122 cites W2058747164 @default.
• W2891941122 cites W2074979486 @default.
• W2891941122 cites W2088325304 @default.
• W2891941122 cites W2092515735 @default.
• W2891941122 cites W2094771953 @default.
• W2891941122 cites W2098241352 @default.
• W2891941122 cites W2100724662 @default.
• W2891941122 cites W2101231029 @default.
• W2891941122 cites W2102034693 @default.
• W2891941122 cites W2104974272 @default.
• W2891941122 cites W2108366680 @default.
• W2891941122 cites W2111388596 @default.
• W2891941122 cites W2113647338 @default.
• W2891941122 cites W2117814597 @default.
• W2891941122 cites W2123193821 @default.
• W2891941122 cites W2128446133 @default.
• W2891941122 cites W2133752904 @default.
• W2891941122 cites W2138033100 @default.
• W2891941122 cites W2142095302 @default.
• W2891941122 cites W2148515475 @default.
• W2891941122 cites W2162377106 @default.
• W2891941122 cites W2162989648 @default.
• W2891941122 cites W2166457346 @default.
• W2891941122 cites W2170677364 @default.
• W2891941122 cites W2304913076 @default.
• W2891941122 cites W2346944018 @default.
• W2891941122 cites W2411767523 @default.
• W2891941122 cites W2412492030 @default.
• W2891941122 cites W2479771048 @default.
• W2891941122 cites W2513602004 @default.
• W2891941122 cites W2581178587 @default.
• W2891941122 cites W2587246820 @default.
• W2891941122 cites W2619451607 @default.
• W2891941122 doi "https://doi.org/10.3389/fcvm.2018.00124" @default.
• W2891941122 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6151311" @default.
• W2891941122 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30276199" @default.
• W2891941122 hasPublicationYear "2018" @default.
• W2891941122 type Work @default.
• W2891941122 sameAs 2891941122 @default.
• W2891941122 citedByCount "39" @default.
• W2891941122 countsByYear W28919411222019 @default.
• W2891941122 countsByYear W28919411222020 @default.
• W2891941122 countsByYear W28919411222021 @default.
• W2891941122 countsByYear W28919411222022 @default.
• W2891941122 countsByYear W28919411222023 @default.
• W2891941122 crossrefType "journal-article" @default.
• W2891941122 hasAuthorship W2891941122A5000015310 @default.
• W2891941122 hasAuthorship W2891941122A5027652711 @default.
• W2891941122 hasAuthorship W2891941122A5031145615 @default.
• W2891941122 hasAuthorship W2891941122A5060547232 @default.
• W2891941122 hasAuthorship W2891941122A5088386918 @default.
• W2891941122 hasBestOaLocation W28919411221 @default.
• W2891941122 hasConcept C105702510 @default.
• W2891941122 hasConcept C126838900 @default.
• W2891941122 hasConcept C142724271 @default.
• W2891941122 hasConcept C164705383 @default.
• W2891941122 hasConcept C2776098176 @default.
• W2891941122 hasConcept C2776716733 @default.
• W2891941122 hasConcept C2777323849 @default.
• W2891941122 hasConcept C2779205420 @default.
• W2891941122 hasConcept C2779869378 @default.
• W2891941122 hasConcept C2779993416 @default.
• W2891941122 hasConcept C2780714102 @default.
• W2891941122 hasConcept C2780847584 @default.
• W2891941122 hasConcept C2781355080 @default.
• W2891941122 hasConcept C71924100 @default.
• W2891941122 hasConcept C99322962 @default.

• next