FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1997123196> ?p ?o ?g. }

• W1997123196 abstract "An accepted hypothesis states that coronary atherosclerosis (CA) is initiated by endothelial dysfunction due to inflammation and high levels of LDL-C, followed by deposition of lipids and macrophages from the luminal blood into the arterial intima, resulting in plaque formation. The success of statins in preventing CA promised much for extended protection and effective therapeutics. However, stalled progress in pharmaceutical treatment gives a good reason to review logical properties of the hypothesis underlining our efforts, and to reconsider whether our perception of CA is consistent with facts about the normal and diseased coronary artery.To begin with, it must be noted that the normal coronary intima is not a single-layer endothelium covering a thin acellular compartment, as claimed in most publications, but always appears as a multi-layer cellular compartment, or diffuse intimal thickening (DIT), in which cells are arranged in many layers. If low density lipoprotein cholesterol (LDL-C) invades the DIT from the coronary lumen, the initial depositions ought to be most proximal to blood, i.e. in the inner DIT. The facts show that the opposite is true, and lipids are initially deposited in the outer DIT. This contradiction is resolved by observing that the normal DIT is always avascular, receiving nutrients by diffusion from the lumen, whereas in CA the outer DIT is always neovascularized from adventitial vasa vasorum. The proteoglycan biglycan, confined to the outer DIT in both normal and diseased coronary arteries, has high binding capacity for LDL-C. However, the normal DIT is avascular and biglycan-LDL-C interactions are prevented by diffusion distance and LDL-C size (20 nm), whereas in CA, biglycan in the outer DIT can extract lipoproteins by direct contact with the blood. These facts lead to the single simplest explanation of all observations: (1) lipid deposition is initially localized in the outer DIT; (2) CA often develops at high blood LDL-C levels; (3) apparent CA can develop at lowered blood LDL-C levels. This mechanism is not unique to the coronary artery: for instance, the normally avascular cornea accumulates lipoproteins after neovascularization, resulting in lipid keratopathy.Neovascularization of the normally avascular coronary DIT by permeable vasculature from the adventitial vasa vasorum is the cause of LDL deposition and CA. DIT enlargement, seen in early CA and aging, causes hypoxia of the outer DIT and induces neovascularization. According to this alternative proposal, coronary atherosclerosis is not related to inflammation and can occur in individuals with normal circulating levels of LDL, consistent with research findings." @default.
• W1997123196 created "2016-06-24" @default.
• W1997123196 creator A5055497627 @default.
• W1997123196 date "2012-04-10" @default.
• W1997123196 modified "2023-10-14" @default.
• W1997123196 title "Neovascularization of coronary tunica intima (DIT) is the cause of coronary atherosclerosis. Lipoproteins invade coronary intima via neovascularization from adventitial vasa vasorum, but not from the arterial lumen: a hypothesis" @default.
• W1997123196 cites W1543809841 @default.
• W1997123196 cites W1543927057 @default.
• W1997123196 cites W1565922087 @default.
• W1997123196 cites W1602214891 @default.
• W1997123196 cites W1609483177 @default.
• W1997123196 cites W1853821798 @default.
• W1997123196 cites W1963840048 @default.
• W1997123196 cites W1966041159 @default.
• W1997123196 cites W1966199777 @default.
• W1997123196 cites W1967703489 @default.
• W1997123196 cites W1971139558 @default.
• W1997123196 cites W1974700560 @default.
• W1997123196 cites W1977820385 @default.
• W1997123196 cites W1981201963 @default.
• W1997123196 cites W1984176331 @default.
• W1997123196 cites W1987232206 @default.
• W1997123196 cites W1987430295 @default.
• W1997123196 cites W1991237283 @default.
• W1997123196 cites W1992033013 @default.
• W1997123196 cites W1992828906 @default.
• W1997123196 cites W1993960003 @default.
• W1997123196 cites W1993997290 @default.
• W1997123196 cites W1994101670 @default.
• W1997123196 cites W1994425929 @default.
• W1997123196 cites W1994710013 @default.
• W1997123196 cites W1995739525 @default.
• W1997123196 cites W1996448555 @default.
• W1997123196 cites W1998181555 @default.
• W1997123196 cites W2000111545 @default.
• W1997123196 cites W2000904460 @default.
• W1997123196 cites W2001500938 @default.
• W1997123196 cites W2009789367 @default.
• W1997123196 cites W2012306318 @default.
• W1997123196 cites W2014193046 @default.
• W1997123196 cites W2014958065 @default.
• W1997123196 cites W2018404713 @default.
• W1997123196 cites W2021939552 @default.
• W1997123196 cites W2023730546 @default.
• W1997123196 cites W2024599560 @default.
• W1997123196 cites W2025057269 @default.
• W1997123196 cites W2026487217 @default.
• W1997123196 cites W2027092108 @default.
• W1997123196 cites W2028817450 @default.
• W1997123196 cites W2029093013 @default.
• W1997123196 cites W2030603652 @default.
• W1997123196 cites W2033390204 @default.
• W1997123196 cites W2033896075 @default.
• W1997123196 cites W2034404961 @default.
• W1997123196 cites W2039970057 @default.
• W1997123196 cites W2047183558 @default.
• W1997123196 cites W2047577073 @default.
• W1997123196 cites W2048874665 @default.
• W1997123196 cites W2050007290 @default.
• W1997123196 cites W2050558646 @default.
• W1997123196 cites W2052568078 @default.
• W1997123196 cites W2053312338 @default.
• W1997123196 cites W2056030287 @default.
• W1997123196 cites W2056132084 @default.
• W1997123196 cites W2056318538 @default.
• W1997123196 cites W2056775084 @default.
• W1997123196 cites W2058970290 @default.
• W1997123196 cites W2061418563 @default.
• W1997123196 cites W2061755142 @default.
• W1997123196 cites W2064988792 @default.
• W1997123196 cites W2066407369 @default.
• W1997123196 cites W2069593788 @default.
• W1997123196 cites W2069648342 @default.
• W1997123196 cites W2070334258 @default.
• W1997123196 cites W2070451449 @default.
• W1997123196 cites W2073162693 @default.
• W1997123196 cites W2073968191 @default.
• W1997123196 cites W2076266099 @default.
• W1997123196 cites W2077646768 @default.
• W1997123196 cites W2077988878 @default.
• W1997123196 cites W2081958468 @default.
• W1997123196 cites W2081985863 @default.
• W1997123196 cites W2083092599 @default.
• W1997123196 cites W2083682299 @default.
• W1997123196 cites W2084616463 @default.
• W1997123196 cites W2085804112 @default.
• W1997123196 cites W2088423156 @default.
• W1997123196 cites W2089121045 @default.
• W1997123196 cites W2093663386 @default.
• W1997123196 cites W2094941678 @default.
• W1997123196 cites W2095426703 @default.
• W1997123196 cites W2098983556 @default.
• W1997123196 cites W2100724662 @default.
• W1997123196 cites W2104974272 @default.
• W1997123196 cites W2107570938 @default.
• W1997123196 cites W2109807835 @default.
• W1997123196 cites W2110100816 @default.
• W1997123196 cites W2111694919 @default.
• W1997123196 cites W2113839948 @default.
• W1997123196 cites W2114124922 @default.

• next