Oxidative Stress and Vascular Disease

  • John F. KeaneyJr.

Part of the Developments in Cardiovascular Medicine book series (DICM, volume 224)

Table of contents

  1. Front Matter
    Pages i-xvii
  2. General Concepts

    1. Front Matter
      Pages 1-1
    2. Helmut Sies
      Pages 1-8
    3. Jay W. Heinecke
      Pages 9-25
    4. Roland Stocker
      Pages 27-47
  3. Atherosclerosis

    1. Front Matter
      Pages 49-49
    2. Sotirios Tsimikas, Joseph L. Witztum
      Pages 49-74
    3. Mark R. McCall, Balz Frei
      Pages 75-98
    4. Sean Davies, Thomas McIntyre, Stephen Prescott, Guy Zimmerman
      Pages 99-118
    5. Norbert Leitinger, Judith A. Berliner
      Pages 119-134
    6. Charles Kunsch, Russell M. Medford
      Pages 135-154
    7. Jane E. Freedman
      Pages 183-194
    8. John F. Keaney Jr.
      Pages 195-211
    9. Elizabeth S. Biegelsen, Joseph A. Vita
      Pages 213-243
    10. J. Michael Gaziano
      Pages 245-258
  4. Diabetes

    1. Front Matter
      Pages 259-259
    2. Suzanne R. Thorpe, Timothy J. Lyons, John W. Baynes
      Pages 259-285

About this book

Introduction

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.

Keywords

atherosclerosis cardiovascular gene gene expression hypertension oxidative stress physiology signal transduction transcription vascular disease

Editors and affiliations

  • John F. KeaneyJr.
    • 1
  1. 1.Boston University School of MedicineBostonUSA

Bibliographic information

  • DOI https://doi.org/10.1007/978-1-4615-4649-8
  • Copyright Information Kluwer Academic Publishers 2000
  • Publisher Name Springer, Boston, MA
  • eBook Packages Springer Book Archive
  • Print ISBN 978-1-4613-7103-8
  • Online ISBN 978-1-4615-4649-8
  • Series Print ISSN 0166-9842
  • About this book