According to the World Health Report (2000 http:/ /www. who. int/whr), of the 55 million deaths worldwide in 1999, more than 16 million were secondary to car diovascular complications. With the prospect of world population increasing from the current level of 6 billion to 9 billion by the middle of this century, the burden of cardiac disease is going to increase astronomically. Furthermore, scientists are being challenged not only to reduce mortality, but also to improve quality of life. Thus, more than ever, intellectuals from different disciplines including biology, sociology, informatics and health care have to join forces to meet the mandate. The World Heart Congress with a focus on "Frontiers in Cardiovascular Health" held in Winnipeg during July 6-11, 2001, made a unique attempt to bring these specialists together to brainstorm and map out the course of action for cardiovascular research and health in the next century. Anytime there is a relative increase in the workload on the heart, there are adap tive myocardial as well as humoral responses. When these adaptations or remodel ing at the organ, subcellular or gene level, become inadequate for a proper tissue perfusion, the condition of heart failure ensues. Prevention of the factors leading to the relative increase in workload as well as a better understanding of the adap tive responses and their failure are some of the hopes to combat the morbidity and mortality due to heart failure.

The focus of this special issue of Molecular and Cellular Biochemistry is underlying mechanisms that regulate cardiac growth. The new information provided in this special issue can be utilized to design new treatment modalities that will reduce the incidence of cardiac failure which will improve quality of life in patients with chronic heart disease.

One of the most intriguing and compelling issues to impact contemporary biology to date is the concept that cell death is genetically regulated. Observations by Kerr and Wyllie, made more than 30 years ago on the basis of distinct morphological criteria, markedly distinguished apoptosis from classical cell death by necrosis. Apoptosis is a highly regulated, evolutionary conserved, genetic program of cell death essential for normal development and tissue homeostasis. The discovery of apoptosis as a regulated event and potentially amenable to therapeutic interventions has generated considerable excitement because it meant that disease entities resulting from either too much, or too little, apoptosis could be potentially cured with new therapies that target apoptosis. While there is little doubt that necrosis induced by massive cellular trauma is likely an unregulated event, several lines of investigation have challenged the dogma that necrotic cell death is merely unregulated. Emerging data has shifted the paradigm in our thinking about necrosis as a regulated event. Autophagy is another cellular process that has received considerable attention over the past two decades and its remarkable involvement in the processes of cell survival, death and tumorigenesis. Macro autophagy is a catabolic process that involves the selective and targeted removal of oxidized proteins, macromolecular structures and organelles through an elaborate cellular process involving a lysosome mediated pathway. Other forms of autophagy involving adapter proteins, commonly referred to as chaperone mediated autophagy, involves the selective removal of cellular cargo by the ubiquitin-proteasome pathway. The book will serve as a reference guide for basic and clinical scientists who are interested in understanding how these critical cellular processes impact the pathogenesis of human disease.