Oxidative Stress and Vascular Disease

Front Cover
John F. Keaney
Springer Science & Business Media, Dec 31, 1999 - Medical - 373 pages
2 Reviews
One 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.
  

What people are saying - Write a review

User Review - Flag as inappropriate

I liked the 2nd chapter
It is lovely and extremely comprehensive the specific mechanism of LDL oxidation was there,
Thanks a lot
Regards,
Yousif Shamsaldeen
 

Contents

WHAT IS OXIDATIVE STRESS?
1
SOURCES OF VASCULAR OXIDATIVE STRESS
9
ANTIOXIDANT DEFENSES IN THE VASCULAR WALL
27
THE OXIDATIVE MODIFICATION HYPOTHESIS OF ATHEROGENESIS
49
MECHANISMS OF LDL OXIDATION
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

Common terms and phrases

Bibliographic information