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OxLDL function

The pathophysiological role of oxidized LDL-induced apoptosis in vessel wall homeostasis is complex and probably depends on the cell type that oxLDL interacts with. For instance, EC are potential early targets, oxidized LDL may alter their functions and lead to apoptosis, contributing to early... [Pg.124]

A corollary of the oxidation hypothesis of atherogenesis is that antioxidants may reduce the progression of the disease (114). Antioxidants present in LDL, including alpha-tocopherol, and antioxidants present in the extracellular fluid of the arterial wall, including ascorbic acid (vitamin C), inhibit LDL oxidation (132), and this action is extended to multiple oxLDL-mediated signaling pathways (133). Vitamin C may potentiate NO activity and normalize vascular function in patients with CHD and classical risk factors (132). Thus, NO may restore endothelial dysfunction and ameliorate vascular remodeling in several clinical correlates to experimental... [Pg.110]

Important evidence for a role of OxPL as modulators of DC function in vivo comes from studies performed in ApoE-deficient mice, which have elevated levels of OxLDL and suffer from severe dyslipidemia and accelerated... [Pg.338]

Peroxidation of unsaturated fatty acids, loss of membrane fluidity/function, OxLDL formation... [Pg.149]

Modulation of the expression and function of vascular graies is yet another effect exerted by oxLDLs by which these genes may participate in inflammatory and atherosclerotic processes. OxLDL increases the VCAM-1 induction response to a cytokine inflammatory signal in endothehal cells from different vaseular beds. More recently, oxLDLs have been shown to stimulate intercellular adhesion molecule (ICAM-1) expression in EC and monocyte adhesion, probably through activation of a speciflc protein tyrosine kinase (PTK). ... [Pg.64]

LDL-C is known to cause numerous cellular changes that contribute to the atherosclerotic process through the subendothelial retention of Apo B 100 containing lipoproteins, followed by biologic responses to the retained material (reviewed in ref. 347). One of the first alterations in EC function induced by LDL-C is an attenuation of endothelial-dependent vasodilation. This reduced responsiveness to vasodilation occurs before any clinical evidence of atherosclerosis. Studies in isolated vessels from normal animals demonstrate a reduction in endothelial-dependent vasodilation within minutes of exposure to oxLDL (348,349). [Pg.131]

In WHHL rabbits, aortic accumulation of hydroxide of CE and TG is not required nor is a-tocopherol depleted during atherosclerosis (385). It was suggested that the atherogenecity of oxLDL in cultured humans aortic SMC is a result of LDL aggregation and not oxidation (386). PC hydroxyalkenals, a class of oxidized PC, are present in vivo and possess multiple functions characteristic of oxLDL and 4-hydroxy nonenal (387). [Pg.134]

Chow, S.E., Hshu, Y.C., Wang, J.S., and Chen, J.K. 2007. Resveratrol attenuates oxLDL-stimulated NADPH oxidase activity and protects endothelial eells from oxidative functional... [Pg.515]

Investigators have shown that a decrease in the release of tissue plasminogen activator (tPA) and an elevation of plasminogen activator inhibitor 1 (PAI-1) will reduce fibrinolytic function. It has emerged that triacylglycerol-rich lipoproteins stimulate PAI-1 secretion from endothelial cells, and furthermore it has been shown that OxLDL induces secretion, whereas native LDL has no detectable... [Pg.166]


See other pages where OxLDL function is mentioned: [Pg.125]    [Pg.129]    [Pg.140]    [Pg.94]    [Pg.125]    [Pg.129]    [Pg.134]    [Pg.135]    [Pg.140]    [Pg.111]    [Pg.334]    [Pg.355]    [Pg.5]    [Pg.13]    [Pg.199]    [Pg.282]    [Pg.284]    [Pg.286]    [Pg.315]    [Pg.317]    [Pg.3683]    [Pg.132]    [Pg.133]    [Pg.147]    [Pg.1]    [Pg.164]   
See also in sourсe #XX -- [ Pg.114 ]




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OxLDL

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