FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W147253478> ?p ?o ?g. }

• W147253478 endingPage "118" @default.
• W147253478 startingPage "99" @default.
• W147253478 abstract "Atherosclerosis has been thought to be an inevitable consequence of aging, but progress in understanding the molecular and pathological basis of this vascular disease through the work of Brown and Goldstein (1) has made it clear that this need not be the case. Specific risk factors for this disease exist, and these elucidate general mechanisms underlying this disease. For example, failure to adequately remove plasma cholesterol in the form of low-density lipoprotein (LDL) from the bloodstream, due to mutations in the LDL receptor, leads to high concentration of plasma LDL that is sufficient to cause the disease. Other work (2) demonstrated that LDL underwent oxidative modification to generate particles that were more effective in causing pathological effects. Elevated levels of LDL promoted this pathologic change. Ross proposed a “response-to-injury” model of atherosclerosis (3), where damage to the vessel wall initiated the disease. A refined version of this model recognizes that the early steps in atherogenesis need not necessarily be initiated by the cytotoxicity of oxidized LDL, but rather by activation of an inflammatory response in vascular tissue. Oxidation inappropriately stimulates the normal inflammatory response of endothelial cells and leukocytes. Activation of this normally tightly regulated inflammatory response program, by factors which themselves are not well regulated, (i.e. oxidation of LDL by uncontrolled chemical reactions) leads to chronic, unregulated inflammation of the vascular wall. Such a chronic inflammatory process remodels the vessel wall, drives plaque formation, and destabilizes plaque structures, all key events in atherosclerosis.KeywordsHuman Umbilical Vein Endothelial CellHuman Endothelial CellLeukocyte Adhesion DeficiencyTumor Necrosis Factor ReleaseDiacyl PhospholipidThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves." @default.
• W147253478 created "2016-06-24" @default.
• W147253478 creator A5002690026 @default.
• W147253478 creator A5019289575 @default.
• W147253478 creator A5053822172 @default.
• W147253478 creator A5090473064 @default.
• W147253478 date "2000-01-01" @default.
• W147253478 modified "2023-09-23" @default.
• W147253478 title "Oxidized Phospholipids as Mediators of Vascular Disease" @default.
• W147253478 cites W1487411642 @default.
• W147253478 cites W1491197989 @default.
• W147253478 cites W1491645799 @default.
• W147253478 cites W1500255296 @default.
• W147253478 cites W1501486266 @default.
• W147253478 cites W1513212892 @default.
• W147253478 cites W1515846068 @default.
• W147253478 cites W1528898535 @default.
• W147253478 cites W1530740124 @default.
• W147253478 cites W1547302919 @default.
• W147253478 cites W1548377812 @default.
• W147253478 cites W1559138834 @default.
• W147253478 cites W1569246394 @default.
• W147253478 cites W1570643773 @default.
• W147253478 cites W1576253698 @default.
• W147253478 cites W1585449429 @default.
• W147253478 cites W1589395925 @default.
• W147253478 cites W1608131589 @default.
• W147253478 cites W1648812418 @default.
• W147253478 cites W1748919512 @default.
• W147253478 cites W1881475207 @default.
• W147253478 cites W188280680 @default.
• W147253478 cites W1893528652 @default.
• W147253478 cites W1965972035 @default.
• W147253478 cites W1967409457 @default.
• W147253478 cites W1967598068 @default.
• W147253478 cites W1967922054 @default.
• W147253478 cites W1972802318 @default.
• W147253478 cites W1974936467 @default.
• W147253478 cites W1976081153 @default.
• W147253478 cites W1977347590 @default.
• W147253478 cites W1977363772 @default.
• W147253478 cites W1977823463 @default.
• W147253478 cites W1978470067 @default.
• W147253478 cites W1978607604 @default.
• W147253478 cites W1987121959 @default.
• W147253478 cites W1988456139 @default.
• W147253478 cites W1988614616 @default.
• W147253478 cites W1994956837 @default.
• W147253478 cites W1999063996 @default.
• W147253478 cites W200003930 @default.
• W147253478 cites W2000181213 @default.
• W147253478 cites W2000769210 @default.
• W147253478 cites W2001519410 @default.
• W147253478 cites W2004088054 @default.
• W147253478 cites W2004145281 @default.
• W147253478 cites W2004611630 @default.
• W147253478 cites W2010757919 @default.
• W147253478 cites W2011785451 @default.
• W147253478 cites W2015781874 @default.
• W147253478 cites W2016253593 @default.
• W147253478 cites W2016993781 @default.
• W147253478 cites W2024597511 @default.
• W147253478 cites W2029392623 @default.
• W147253478 cites W2030140594 @default.
• W147253478 cites W2030148186 @default.
• W147253478 cites W2032786707 @default.
• W147253478 cites W2035905848 @default.
• W147253478 cites W2036852690 @default.
• W147253478 cites W2037986253 @default.
• W147253478 cites W2043934481 @default.
• W147253478 cites W2045147217 @default.
• W147253478 cites W2046628450 @default.
• W147253478 cites W2048249323 @default.
• W147253478 cites W2049007654 @default.
• W147253478 cites W2049116365 @default.
• W147253478 cites W2052320628 @default.
• W147253478 cites W2054067372 @default.
• W147253478 cites W2055515604 @default.
• W147253478 cites W2057943924 @default.
• W147253478 cites W2061755142 @default.
• W147253478 cites W2062821907 @default.
• W147253478 cites W2063559998 @default.
• W147253478 cites W2064009756 @default.
• W147253478 cites W2067190758 @default.
• W147253478 cites W2070233666 @default.
• W147253478 cites W2078595704 @default.
• W147253478 cites W2079926187 @default.
• W147253478 cites W2080442033 @default.
• W147253478 cites W2084788087 @default.
• W147253478 cites W2085304257 @default.
• W147253478 cites W2089753337 @default.
• W147253478 cites W2092216620 @default.
• W147253478 cites W2093049246 @default.
• W147253478 cites W2100668681 @default.
• W147253478 cites W2106489698 @default.
• W147253478 cites W2118990153 @default.
• W147253478 cites W2121121770 @default.
• W147253478 cites W2121841958 @default.

• next