Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2011:2011:724080.
doi: 10.4061/2011/724080. Epub 2011 Nov 30.

Roles of TGF-β signals in endothelial-mesenchymal transition during cardiac fibrosis

Yasuhiro Yoshimatsu  1 , Tetsuro Watabe
Affiliations

Roles of TGF-β signals in endothelial-mesenchymal transition during cardiac fibrosis

Yasuhiro Yoshimatsu et al. Int J Inflam. 2011.

Abstract

Most cardiac diseases caused by inflammation are associated with fibrosis in the heart. Fibrosis is characterized by the accumulation of fibroblasts and excess deposition of extracellular matrix (ECM), which results in the distorted organ architecture and function. Recent studies revealed that cardiac fibroblasts are heterogeneous with multiple origins. Endothelial-mesenchymal transition (EndMT) plays important roles in the formation of cardiac fibroblasts during pathological settings. EndMT is regulated by signaling pathways mediated by cytokines including transforming growth factor (TGF)-β. Better understanding of the mechanisms of the formation of cardiac fibroblasts via EndMT may provide an opportunity to develop therapeutic strategies to cure heart diseases.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Schematic representation of mesenchymal transition of epithelial (a) and endothelial (b) cells.
Figure 2
Figure 2
Smad signal transduction pathways mediated by TGF-β and BMP family members.
Figure 3
Figure 3
Non-Smad signal transduction pathways mediated by TGF-β family members.
See this image and copyright information in PMC

References

    1. Zeisberg EM, Tarnavski O, Zeisberg M, et al. Endothelial-to-mesenchymal transition contributes to cardiac fibrosis. Nature Medicine. 2007;13(8):952–961. - PubMed
    1. Dettman RW, Denetclaw W, Ordahl CP, Bristow J. Common epicardial origin of coronary vascular smooth muscle, perivascular fibroblasts, and intermyocardial fibroblasts in the avian heart. Developmental Biology. 1998;193(2):169–181. - PubMed
    1. Manner J. Does the subepicardial mesenchyme contribute myocardioblasts to the myocardium of the chick embryo heart? A quail-chick chimera study tracing the fate of the epicardial primordium. Anatomical Record. 1999;255(2):212–226. - PubMed
    1. Peeters MPFMV, Gittenberger-de Groot AC, Mentink MMT, Poelmann RE. Smooth muscle cells and fibroblasts of the coronary arteries derive from epithelial-mesenchymal transformation of the epicardium. Anatomy and Embryology. 1999;199(4):367–378. - PubMed
    1. Rivera-Feliciano J, Lee KH, Kong SW, et al. Development of heart valves requires Gata4 expression in endothelial-derived cells. Development. 2006;133(18):3607–3618. - PMC - PubMed

LinkOut - more resources