Abstract
Cardiac fibroblasts are the major nonmuscle cells of ventricular myocardium, where they comprise up to 30% of the total cell population of the murine heart [ [1] Banerjee I. Fuseler J.W. Price R.L. Borg T.K. Baudino T.A. Determination of cell types and numbers during cardiac development in the neonatal and adult rat and mouse. Am J Physiol Heart Circ Physiol. 2007; 293: H1883-H1891 Crossref PubMed Scopus (450) Google Scholar ]. Their lineage remains uncertain, although their ancestry appears to be derived from multiple sources during development and disease [ 2 Zeisberg E.M. Kalluri R. Origins of cardiac fibroblasts. Circ Res. 2010; 107: 1304-1312 Crossref PubMed Scopus (174) Google Scholar , 3 Krenning G. Zeisberg E.M. Kalluri R. The origin of fibroblasts and mechanism of cardiac fibrosis. J Cell Physiol. 2010; 225: 631-637 Crossref PubMed Scopus (452) Google Scholar ]. Cardiac fibroblasts are the major producers of extracellular matrix (ECM) proteins, and as such have been implicated as the predominant cell type responsible for the interstitial and perivascular fibrosis that develops during ventricular remodeling [ [4] Eleftheriades E.G. Durand J.B. Ferguson A.G. Engelmann G.L. Jones S.B. Samarel A.M. Regulation of procollagen metabolism in the pressure-overloaded rat heart. J Clin Invest. 1993; 91: 1113-1122 Crossref PubMed Scopus (58) Google Scholar ]. As fibroblast lineage varies, it remains unclear whether all subpopulations of cardiac fibroblasts participate in the over-production of fibrillar collagens and other ECM components during cardiac fibrosis. Nevertheless, a complete understanding on the molecular mechanisms responsible for cardiac fibrosis may provide new avenues for therapeutic intervention in heart failure. In a recent issue of the Journal, Herum and colleagues [ [5] Herum K.M. Lunde I.G. Skrbic B. Florholmen G. Behmen D. Sjaastad I. et al. Syndecan-4 signaling via NFAT regulates extracellular matrix production and cardiac myofibroblast differentiation in response to mechanical stress. J Mol Cell Cardiol. 2013; 54: 73-81 Abstract Full Text Full Text PDF PubMed Scopus (102) Google Scholar ] now provide new and important information regarding the phenotypic modulation of cardiac fibroblasts, and reveal a previously unrecognized signaling pathway involved in the regulation of cardiac ECM biosynthesis.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
