Tenascin-C (TNC) is a large extracellular matrix (ECM)
glycoprotein and an original member of the matricellular
protein family. TNC is transiently expressed in the heart during embryonic development, but is rarely detected in normal adults; however, its expression is strongly up-regulated with
inflammation. Although neither TNC-knockout nor -overexpressing mice show a distinct phenotype, disease models using genetically engineered mice combined with in vitro experiments have revealed multiple significant roles for TNC in responses to injury and myocardial repair, particularly in the regulation of
inflammation. In most cases, TNC appears to deteriorate adverse
ventricular remodeling by aggravating
inflammation/
fibrosis. Furthermore, accumulating clinical evidence has shown that high TNC levels predict adverse
ventricular remodeling and a poor prognosis in patients with various
heart diseases. Since the importance of
inflammation has attracted attention in the pathophysiology of
heart diseases, this review will focus on the roles of TNC in various types of inflammatory reactions, such as
myocardial infarction, hypertensive
fibrosis,
myocarditis caused by
viral infection or autoimmunity, and
dilated cardiomyopathy. The utility of TNC as a
biomarker for the stratification of
myocardial disease conditions and the selection of appropriate
therapies will also be discussed from a clinical viewpoint.