Heart failure (HF) is a feared endpoint for most cardiovascular diseases and is a major cause of morbidity and mortality. The worldwide prevalence of HF is between 2 and 3 % and rises sharply at around 75 years of age, so that the prevalence in 70- to 80-year-old people is between 10–20 %. With a 50 % 5-year survival rate, HF is predicted to be the leading cause of all morbidity by 2020.1,2 Despite the varied etiologies, ventricular dysfunction is ultimately the result of pathologic cardiac remodelling. Cardiac remodelling is defined as a series of compensatory alterations in the size, shape, and function of the myocardium in response to cardiac injury with the aim being to restore cardiac output. However, if this process continues, chronic cardiac stress magnifies maladaptive mechanisms, including cardiac hypertrophy, fibrosis, ventricular dilatation, alteration in geometry, chronic inflammation and increased cellular apoptosis, leading to a vicious cycle of deterioration of cardiac function and worsening of HF.3
The remodelling process involves the permanent cell types of the myocardium, namely the myocytes, the fibroblasts, the endothelial cells, the smooth muscle cells and the stem cells, but also transient cell populations such as immune and circulating stem cells.4 While the cardiac myocyte (CM) has been the focus of most HF research to date, increasing evidence has implicated the cardiac fibroblast (CF) as a key pathologic determinant in cardiac remodelling in both ventricles and atria.5 Dynamic interactions among the different cardiac cell populations via mechanical, chemical and electrical means, as well as their interactions with the extracellular matrix (ECM) determine cardiac physiology and pathology.4,5 Better understanding of these cell-to-cell and cell-to-ECM communications may provide potential novel therapeutic targets for the treatment of HF. In this review, the authors aim to explore the contribution of cellular cross-talk in the cardiac remodelling process.