Heart failure afflicts about 5 million people and causes 300 000 deaths a year in the United States alone [1]. Causes leading to heart failure are cardiac remodeling and signaling events which happen through the progression of disease. Cardiac remodeling is a sum of responses of the heart to conditions such as ischemia, myocardial infarction, volume and pressure overload, infections, inflammation and mechanical injury. These responses, including cardiomyocyte hypertrophy and myocardial fibrosis involve numerous cellular and structural changes, which result in a progressive decline in cardiac performance.
Cardiac performance is ability of heart to supply sufficient blood flow to meet the body's needs. These performance measured by myocardial contractility, ability of the heart to contract independent of preload and afterload. Heart failure is characterized by a progressive loss in contractility and ejection fraction, ventricular chamber dilation, ventricular wall thinning, increased peripheral vascular resistance, and deregulated fluid homeostasis [2]. The molecular mechanism regulating cardiac contractility has been the subject of intense investigation for several decades, however still there are many unanswered questions.
These days pharmacological and genetic approaches using to identify the molecular and cellular mechanisms leading to the disease. Protein kinase C (PKC) isozymes, a family of serine-threonine protein kinase enzymes, were found to regulate a number of cardiac responses, including those associated with heart failure [1]. PKC is an enzyme involved in the differentiation and proliferation of a variety of cells and exists as a family of 11 isozymes. PKC classified as (1) the classical PKCs (, , , and ), the diacylglycerol (DAG)-, and calcium-dependent enzymes, (2) the novel PKCs (), which require DAG, but not calcium, for activity, and (3) the atypical PKCs (), which are not stimulated by DAG or calcium, but are stimulated...