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. Author manuscript; available in PMC: 2015 Apr 27.
Published in final edited form as: Physiol Rev. 2012 Apr;92(2):635–688. doi: 10.1152/physrev.00008.2011

Figure 9. The role of SPARC in cardiac remodeling.

Figure 9

A. SPARC upregulation in the infarcted mouse myocardium. B-D. SPARC null mice have increased incidence of cardiac rupture (C, arrow), exhibiting intramural hemorrhages in the infarcted myocardium (D, arrows). Data reproduced with permission from: Schellings MW, Vanhoutte D, Swinnen M, Cleutjens JP, Debets J, van Leeuwen RE, d’Hooge J, Van de Werf F, Carmeliet P, Pinto YM, Sage EH, Heymans S. Absence of SPARC results in increased cardiac rupture and dysfunction after acute myocardial infarction. J Exp Med 2009;206:113–123: Copyright 2009, Rockefeller University Press. E. The SPARC molecule contains an acidic region, a follistatin-like domain and an extracellular Ca2+-binding region (EC-module). F. The mechanisms involved in SPARC-mediated cardiac fibrosis are likely due to enhanced growth factor signaling and to effects on matrix assembly, MMP activity and fibroblast function.