FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2144294129> ?p ?o ?g. }

• W2144294129 abstract "Atherosclerosis and arterial remodeling Atherosclerosis is a chronic inflammatory disease and the primary cause of cardiovascular events like myocardial infarction. Based on plaque composition, stable and unstable atherosclerotic lesions are discriminated. Unstable lesions are prone to rupture and subsequent thrombus formation often results in acute occlusion of the artery. The size of the lumen of an atherosclerotic artery is determined by the atherosclerotic lesion, together with arterial remodeling. In early stages of atherosclerosis, outward arterial remodeling compensates for lumen loss due to plaque formation. However, in advanced atherosclerotic lesions, outward arterial remodeling is associated with rupture prone lesions. Inflammation and immune responses are involved in the initiation and progression of atherosclerotic disease. The immune system responds effectively to harmful agents by close interplay between the innate and adaptive immune systems. The innate immune response is the first line of defense against invading pathogens. Immune cells recognize pathogens via pattern recognition receptors, including scavenger receptors and Toll-like receptors. B- and T- cells are involved in the highly specific adaptive immune response. Toll-like receptors Toll-like receptors are not only expressed by immune cells, but also by vascular cells. In healthy arteries TLR4 is expressed in low levels. In atherosclerotic lesions, however, TLR4 expression is markedly increased. TLR4 is involved in intima formation and vulnerability for the development of carotid atherosclerosis. Whether TLR4 is also involved in arterial remodeling, the other determinant of lumen loss is investigated in this thesis. The Toll-like receptor 4 signaling in arterial remodeling We demonstrated that TLR4 is involved in outward arterial remodeling both with and without intima formation. TLR4 expression is upregulated during outward remodeling. TLR activation results in translocation of NF-?B into the nucleus and transcription of inflammatory genes. Downstream of TLR4, we investigated the role of NF-?B p50 in arterial remodeling. The p50 subunit is known as a regulatory subunit of NF-?B signaling. In our study, targeted deletion of the regulatory NF-?B p50 subunit enhanced flow-induced outward arterial remodeling. During outward arterial remodeling, levels of endogenous TLR4 ligands EDA and HSP60 are increased. Extra Domain A is incorporated in fibronectin during embryogenesis, wound healing, cellular damage and atherogenesis. We demonstrated a role of EDA in the process of outward remodeling, probably due to the diminished migration capacity of cells without EDA. Endogenous Toll-like receptor 4 ligand EDA in atherosclerosis Higher EDA levels are detected stable human atherosclerotic plaques. This observation implies that the detection of an endogenous TLR4 ligand not necessarily represent an inflammatory environment destabilizing the vulnerable plaque, but also may trigger the stabilization of atherosclerotic lesions. Interaction between Toll-like receptor 4 and Transforming Growth Factor ? signaling We found an association of endogenous TLR4 ligand EDA with Endoglin, an accessory receptor of TGF? in atherosclerotic lesions. This suggests communication between TLR4 and TGF pathways in atherosclerotic lesions. In monocytes, several sets of mRNAs are regulated by both TLR4 and TGF? stimulation and these mRNAs may play an important role in the progression of atherosclerotic disease leading to clinical events." @default.
• W2144294129 created "2016-06-24" @default.
• W2144294129 creator A5009475257 @default.
• W2144294129 date "2009-01-27" @default.
• W2144294129 modified "2023-09-28" @default.
• W2144294129 title "Toll-like receptor 4 signaling in atherosclerotic disease, atherosclerosis, arterial remodeling, cross-talk" @default.
• W2144294129 cites W1455203126 @default.
• W2144294129 cites W1483162601 @default.
• W2144294129 cites W1495287184 @default.
• W2144294129 cites W1520365933 @default.
• W2144294129 cites W1531761590 @default.
• W2144294129 cites W1537033121 @default.
• W2144294129 cites W1560201422 @default.
• W2144294129 cites W1591714343 @default.
• W2144294129 cites W165176759 @default.
• W2144294129 cites W165654455 @default.
• W2144294129 cites W1760966156 @default.
• W2144294129 cites W1768438545 @default.
• W2144294129 cites W1965315844 @default.
• W2144294129 cites W1966071013 @default.
• W2144294129 cites W1966296687 @default.
• W2144294129 cites W1968143482 @default.
• W2144294129 cites W1968567802 @default.
• W2144294129 cites W1970017835 @default.
• W2144294129 cites W1971910601 @default.
• W2144294129 cites W1974083788 @default.
• W2144294129 cites W1978926805 @default.
• W2144294129 cites W1979978633 @default.
• W2144294129 cites W1980790180 @default.
• W2144294129 cites W1984561531 @default.
• W2144294129 cites W1991731944 @default.
• W2144294129 cites W1991998151 @default.
• W2144294129 cites W1992565802 @default.
• W2144294129 cites W1993966022 @default.
• W2144294129 cites W1996133970 @default.
• W2144294129 cites W1999916897 @default.
• W2144294129 cites W2000352826 @default.
• W2144294129 cites W2003219549 @default.
• W2144294129 cites W2004121042 @default.
• W2144294129 cites W2004568153 @default.
• W2144294129 cites W2005047699 @default.
• W2144294129 cites W2005445619 @default.
• W2144294129 cites W2008907994 @default.
• W2144294129 cites W2010701664 @default.
• W2144294129 cites W2010791052 @default.
• W2144294129 cites W2010866783 @default.
• W2144294129 cites W2013914418 @default.
• W2144294129 cites W2014932670 @default.
• W2144294129 cites W2018128871 @default.
• W2144294129 cites W2018788678 @default.
• W2144294129 cites W2019825630 @default.
• W2144294129 cites W2020310192 @default.
• W2144294129 cites W2020546717 @default.
• W2144294129 cites W2022647194 @default.
• W2144294129 cites W2026518217 @default.
• W2144294129 cites W2030237203 @default.
• W2144294129 cites W2031805948 @default.
• W2144294129 cites W2032440984 @default.
• W2144294129 cites W2034523856 @default.
• W2144294129 cites W2037777353 @default.
• W2144294129 cites W2040807303 @default.
• W2144294129 cites W2042783733 @default.
• W2144294129 cites W2045384882 @default.
• W2144294129 cites W2046967596 @default.
• W2144294129 cites W2047617771 @default.
• W2144294129 cites W2049554088 @default.
• W2144294129 cites W2051093466 @default.
• W2144294129 cites W2051942552 @default.
• W2144294129 cites W2053984681 @default.
• W2144294129 cites W2058777468 @default.
• W2144294129 cites W2060372234 @default.
• W2144294129 cites W2063887943 @default.
• W2144294129 cites W2064538798 @default.
• W2144294129 cites W2065988977 @default.
• W2144294129 cites W2066188919 @default.
• W2144294129 cites W2066963386 @default.
• W2144294129 cites W2066964364 @default.
• W2144294129 cites W2067150844 @default.
• W2144294129 cites W2071796176 @default.
• W2144294129 cites W2073426547 @default.
• W2144294129 cites W2073751205 @default.
• W2144294129 cites W2076297716 @default.
• W2144294129 cites W2080568372 @default.
• W2144294129 cites W2081182178 @default.
• W2144294129 cites W2083536576 @default.
• W2144294129 cites W2083709056 @default.
• W2144294129 cites W2084473102 @default.
• W2144294129 cites W2084600823 @default.
• W2144294129 cites W2085263139 @default.
• W2144294129 cites W2085963067 @default.
• W2144294129 cites W2086801198 @default.
• W2144294129 cites W2087175050 @default.
• W2144294129 cites W2090628857 @default.
• W2144294129 cites W2091203739 @default.
• W2144294129 cites W2091637617 @default.
• W2144294129 cites W2091979794 @default.
• W2144294129 cites W2092054266 @default.
• W2144294129 cites W2096086623 @default.
• W2144294129 cites W2100190333 @default.
• W2144294129 cites W2101615512 @default.

• next