Preface

Chapter 7 **MicroRNAome of Vascular Smooth Muscle Cells: Potential for**

Chapter 8 **Atherosclerosis-Susceptible and Atherosclerosis-Resistant**

J. L. Anderson, S. C. Smith and R. L. Taylor Jr.

Veronika A. Myasoedova and Yuri V. Bobryshev

Chapter 10 **Self-Management Training for Chronic Stable Angina: Theory,**

M.H. McGillion, S. O'Keefe-McCarthy and S.L. Carroll

Chapter 11 **Attributes of Hypoxic Preconditioning Determine the Complicating Atherogenesis of Plaques 237**

**Anti-Atherosclerotic Therapy 187**

**Process, and Outcomes 219**

Kasturi Ranganna, Omana P. Mathew, Shirlette G. Milton and

**Pigeon Aortic Smooth Muscle Cells Express Different Genes and**

Alexander N. Orekhov, Igor A. Sobenin, Alexandra A. Melnichenko,

**MicroRNA-Based Vascular Therapies 147**

Barbara E. Hayes

**VI** Contents

**Proteins in vitro 165**

Chapter 9 **Use of Natural Products for Direct**

Lawrence M Agius

Cardiovascular diseases and atherogenesis have been and still are an important topic many scientists are working on.

In the 16th century, Leonardo da Vinci had described "The narrowing of the passage of blood vessels, thickening of the coats of these vessels and hardening of arteries". This is the first documentation of atherosclerosis, but today our understanding of atherogenesis as a process of a chronic inflammatory disease has been updated by many mechanisms such as hypercholesterolemia, dysfunction of endothelial cells, oxidation of lipoproteins and espe‐ cially oxidative stress. In particular, the endothelium is responsible for the regulation of vas‐ cular tone, the exchange of plasma and cell biomolecules, inflammation, lipid metabolism and modulation of fibrinolysis and coagulation. Endothelial cell disruption, morphological abnormalities in size and shape, susceptibility to apoptosis and abnormal release of endo‐ thelial cell-derived factors are strictly implicated in the pathogenetic mechanisms of cardio‐ vascular diseases. Growing evidence indicates that chronic and acute overproduction of oxidative stress alters endothelial cells as pivotal early event in atherogenesis.

It is important to remember that drugs intake, such as statins, life style control for regulating fat intake and exercise activity must be monitored for improving cardiovascular disease in‐ cidence. In recent years a novel topic regarding antioxidant properties of some natural sub‐ stances seems to be very important for decreasing certain problems related to cardiovascular diseases and atherogenesis.

This book presents the state of the art of the antioxidants in the clinical and experimental approaches in order to bring better understanding of the mechanisms and useful therapies for these diseases. We hope that it can indicate new "current trends" for identifying new aspects regarding this scientific problem involving not only anatomical and functional, but also clinical questions.

> **Dr. Rita Rezzani** University of Brescia Italy

**Chapter 1**

**Atherosclerosis and Current Anti-Oxidant**

Cardiovascular diseases (CVDs) remain the leading cause of death in modern societies. The primary cause of dramatic clinical events of CVDs, such as unstable angina, myocardial in‐

The pathophysiological mechanisms of atherosclerosis are complicated and the integrated picture of the disease process is not yet complete, so currently is largely investigated. It is widely recognized that oxidative stress, lipid deposition, inflammation, Vascular smooth muscle cells (VSMCs) differentiation and endothelial dysfunction play a critical role in the formation, progression and eventually rupture of the atherosclerotic plaque [4]. Multiple risk factors have been associated with the development of atherosclerotic lesions; these include diabetes mellitus, hypertension, obesity and tobacco smoking. The risk factors are influenced by genetic predisposition, but also by environmental factors, particularly diet. Moreover, ag‐ ing promotes physiological changes, such as oxidative stress, inflammation and endothelial

The common belief that signs of atherosclerosis and CVDs are clinically relevant only dur‐ ing adult and elderly age is gradually changing, increasing evidence supports that athero‐

Low-density lipoproteins (LDL) are crucial to the development of atherosclerotic lesions, whereas high-density lipoproteins (HDL) are inhibitors of the process, primarily through the process of reverse cholesterol transport [4,7]. Dysfunctional lipid homeostasis plays a central role in the initiation and progression of atherosclerotic lesions. Oxidized-LDL (ox-LDL) induces endothelial dysfunction with focal inflammation which causes increased ex‐ pression of atherogenic signaling molecules that promote the adhesion of monocytes and T

and reproduction in any medium, provided the original work is properly cited.

© 2013 Fabrizio Rodella and Favero; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution,

dysfunction strictly associated with the pathophysiology of atherosclerosis [5].

**Strategies for Atheroprotection**

Additional information is available at the end of the chapter

farction and stroke, is the atherosclerotic process [1,2,3].

Luigi Fabrizio Rodella and Gaia Favero

http://dx.doi.org/10.5772/53035

genesis is initiated in childhood [6].

**1. Introduction**
