Despite excellent diagnostic and therapeutic strategies, hypertensive heart disease is still an important cause of heart failure.1 In response to pressure overload, changes occur in the myocardial architecture, including hypertrophic and fibrotic remodeling. Initially, this augments cardiac performance. However, unbalanced remodeling over protracted periods of cardiac stress eventually leads to heart failure through mechanisms that remain poorly understood.
During the last decade, it has become clear that the cardiac extracellular matrix (ECM) not only acts as structural support but also provides a unique environment in which the embedded cells communicate and function.1,2 By activating signaling cascades, the ECM transduces extracellular changes into cellular and acellular responses that play central roles during cardiac health and disease. In that respect, we have witnessed increasing interest in a group of nonstructural ECM proteins, known as “matricellular proteins.”2,3 Expression of matricellular proteins, including thrombospondins, osteopontin, tenascins, periostin, secreted protein acidic and rich in cysteine, and others, is high during embryogenesis but almost absent during normal postnatal life. Interestingly, they dramatically reappear in response to cardiac injury, stress, or acute remodeling events where they all seem to exhibit critical cardioprotective roles through the regulation of a broad range of ECM and ECM-cell mediated processes.2,3 Together, this has made research in this area attractive at the molecular, cellular, and therapeutic levels.