Oxidative Stress and Vascular DiseaseOne of the major biomedical triumphs of the post-World War II era was the defmitive demonstration that hypercholesterolemia is a key causative factor in atherosclerosis; that hypercholesterolemia can be effectively treated; and that treatment significantly reduces not only coronary disease mortality but also all cause mortality. Treatment to lower plasma levels of cholesterol - primarily low density lipoprotein (LDL) cholesterol - is now accepted as best medical practice and both physicians and patients are being educated to take aggressive measures to lower LDL. We can confidently look forward to important decreases in the toll of coronary artery disease over the coming decades. However, there is still uncertainty as to the exact mechanisms by which elevated plasma cholesterol and LDL levels initiate and favor the progression of lesions. There is general consensus that one of the earliest responses to hypercholesterolemia is the adhesion of monocytes to aortic endothelial cells followed by their penetration into the subendothelial space, where they differentiate into macrophages. These cells, and also medial smooth muscle cells that have migrated into the subendothelial space, then become loaded with mUltiple, large droplets of cholesterol esters . . . the hallmark of the earliest visible atherosclerotic lesion, the so-called fatty streak. This lesion is the precursor of the more advanced lesions, both in animal models and in humans. Thus the centrality of hypercholesterolemia cannot be overstated. Still, the atherogenic process is complex and evolves over a long period of time. |
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I liked the 2nd chapter
It is lovely and extremely comprehensive the specific mechanism of LDL oxidation was there,
Thanks a lotRegards,
Yousif Shamsaldeen
Contents
| 1 | |
| 9 | |
| 27 | |
| 49 | |
| 75 | |
OXIDIZED PHOSPHOLIPIDS AS MEDIATORS OF VASCULAR DISEASE | 99 |
MMLDL AND ATHEROGENESIS A MAJOR ROLE FOR PHOSPHOLIPID OXIDATION PRODUCTS | 119 |
OXIDATIONSENSITIVE TRANSCRIPTION AND GENE EXPRESSION IN ATHEROSCLEROSIS | 135 |
HUMAN STUDIES OF ANTIOXIDANTS AND VASCULAR FUNCTION | 213 |
ANTIOXIDANTS AND CARDIOVASCULAR DISEASE | 245 |
GLYCATION AND GLYCOXIDATION IN DIABETIC VASCULAR DISEASE | 259 |
ADVANCED GLYCOSYLATION ENDPRODUCTS AND DIABETIC VASCULAR DISEASE | 287 |
HYPERGLYCEMIA AND DIABETESINDUCED VASCULAR DYSFUNCTION ROLE OF OXIDATIVE STRESS | 305 |
THE ROLE OF OXIDATIVE STRESS IN HYPERTENSION | 323 |
PROTEIN KINASES THAT MEDIATE REDOXSENSITIVE SIGNAL TRANSDUCTION | 335 |
ANTIOXIDANTS AND RESTENOSIS ANIMAL AND CLINICAL STUDIES | 349 |
ATHEROSCLEROSIS OXIDATIVE STRESS AND ENDOTHELIAL FUNCTION | 155 |
OXIDANTS AND ANTIOXIDANTS IN PLATELET FUNCTION | 183 |
ANTIOXIDANTS AND ATHEROSCLEROSIS ANIMAL STUDIES | 195 |
INDEX | 361 |
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Common terms and phrases
a-tocopherol activity addition adhesion AGEs aminoguanidine animals antioxidant artery ascorbic acid associated atherogenesis atherosclerosis atherosclerotic lesions binding bioactivity Biochem Biol Chem biological blood changes cholesterol Circulation Clin Invest clinical concentrations contribute decreased demonstrated diabetic diet disease effect endothelial cells endothelium endothelium-derived relaxing factor enhanced evidence expression factor formation function gene glucose glutathione glycation glycosylation human impaired important increased induced inhibit intracellular involved kinase LDL oxidation levels lipid peroxidation low density lipoprotein macrophages mechanisms mediated metal mice models modification monocyte myocardial infarction Natl Acad Sci nitric oxide normal observed oxidative stress oxidized LDL oxLDL pathway patients phospholipids plasma platelet potential prevention probucol Proc Natl production protection protein rabbits radical reaction recent receptor reduced regulation relaxation response risk role shown signal smooth muscle cells specific stimulated studies suggest superoxide tissue treatment trials vascular vitamin vitro vivo wall
Popular passages
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Page 94 - Steinbrecher UP, Parthasarathy S. Leake DS, Witztum JL, Steinberg D Modification of low density lipoprotein by endothelial cells involves lipid peroxidation and degradation of low density lipoprotein phospholipids.
Page 42 - Steinberg D, Parthasarathy S, Carew TE, Khoo JC, Witztum JL. Beyond cholesterol. Modifications of low-density lipoprotein that increase its atherogenicity.
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Bibliographic information
| Title | Oxidative Stress and Vascular Disease Volume 224 of Developments in Cardiovascular Medicine |
| Author | John F. Keaney Jr. |
| Edition | illustrated |
| Publisher | Springer Science & Business Media, 1999 |
| ISBN | 0792386787, 9780792386780 |
| Length | 373 pages |
| Subjects | › Medical / Cardiology Medical / Clinical Medicine |
| Export Citation | BiBTeX EndNote RefMan |