Editorial [Hot Topic: Metabolic Syndrome in an Asian Chinese Population and Agents and Targets for Cardiovascular Protection (Guest Editors: M.L. Fung and T.M. Wong)]

INTRODUCTION/SYNOPSIS OF THE SPECIAL ISSUE: Cardiovascular Risk Factors and Metabolic Syndrome in Cardiovascular Diseases Cardiovascular disease is the leading cause of morbidity and mortality in the world and is on an alarming rise in Asian Chinese populations. Risk factors are commonly associated with the dietary habit and lifestyle in the population such as fat consumption, smoking, and also factors including hypertension, hyperlipidemia, which are particularly common in subjects with metabolic syndrome and diabetes. With reference to recommendations focusing on reducing dietary saturated fat, in Asia, however, the problem may not be eating excessive meat but an over intake of calories leading to abdominal obesity, insulin resistance, diabetes, hypertension and the metabolic syndrome. Additionally, the prevalence of the disease grows partly because of the rising numbers in the elderly populations worldwide, particularly noticeable in the Asia. In the first part of this special thematic issue, Cheung and Thomas review the literature and recent studies focusing on the profile of the risk factors in Asian Chinese populations. These are followed by reviews by Thomas and his colleagues and Tan, respectively, on the dietary intervention and the management of dyslipidaemia in the metabolic syndrome. It is shown that a healthy diet early on in life may prevent the development of cardiovascular disease; even in those who already have clinically overt cardiovascular disease. The reviews also highlight on the roles of therapeutic lifestyle modification and drug therapies. Cardiovascular Protection: Approaches to Prevent and Treat Cardiovascular Diseases Cellular and molecular activities induced by cardiovascular stress are the major local events for the protective/compensatory responses or else for the pathogenesis. The second part of this issue aims at reviewing some of the recently-identified mechanisms relevant to the agents and targets proposed for cardiovascular protection. Metabolic nuclear receptors are a group of nuclear hormone receptor transcription factors and play important roles in lipid metabolism, tissue inflammation and remodeling. These receptors such as the peroxisome proliferator-activated receptors have been shown to be involved in pathogenesis of atherosclerosis and ligands for some of the receptors are effective in treating patients with disorders associated with metabolic syndrome. In addition, recent evidence reviewed by Wang suggests modulation of the metabolic nuclear receptors could have potential therapeutic values in treating obesity, hypertension and albuminuria. Moreover, there are circulating substances that can confer cardiovascular protection. Sex hormones are among those agents, which have been shown to have beneficial effects on heart and vessels. Interestingly, in addition to the female hormones, recent literature reviewed by Wong suggests that testosterone can exert a good degree of cardioprotective actions. Intriguingly, the level of testosterone declines in the aging group, which is closely correlated to a rising trend of cardiovascular risk in the elderly male population. Another approach is to target factors known to be involved in the pathogenesis of cardiovascular diseases so as to protect the cardiovascular functions in adverse conditions. Novel targets recently identified are highlighted in this thematic review for extrapolating the therapeutic values of the targets. Experimental studies have demonstrated that ATP-binding cassete transporter-1 (ABCA1) is involved in lipid transportation from cells to apolipoprotein and in cholesterol homeostasis and atherogenic events. Recent evidence reviewed by Zhu suggests oxidized LDL can lower the level of ABCA1, contributing to endothelial dysfunction and plaque formation. Moreover, lesions in the microvessels associated with hyperglycemia that can contribute to the pathogenesis of atherosclerosis by oxidative stress and formation of glycation end product.