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Editorial
. 2008 Oct 21;118(17):1694-6.
doi: 10.1161/CIRCULATIONAHA.108.809475.

Vascularization as a potential enemy in valvular heart disease

Jun Yoshioka, Richard T Lee
Editorial

Vascularization as a potential enemy in valvular heart disease

Jun Yoshioka et al. Circulation. .
No abstract available

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Figures

Figure 1
Figure 1
(A) Schematic structure of human tenomodulin protein. The protein consists mainly of three domains; type II transmembrane domain at the N-terminus (Ile31-Lys51), a BRICHOS domain (Gly93-Ile186), and a cysteine-rich domain at the C-terminus (Phe255-Val317). There are two N-glycosylation sites within the BRICHOS domain, and the potential cleaved site (Arg-Xxx-Xxx-Arg) is located at position 233–236. The cysteine (Cys) rich domain contains eight cysteine residues. The C-terminal domain has a robust anti-angiogenic activity when expressed in a secreted form. (B) Schematic images of normal and pathogenic chordae tendineae. Cross-sectioned chordae show layers of endothelial cells on a basal lamina, the underlying layer consisting of collagen with occasional elastic fibers. Tenomodulin maintains a state of avascularity in healthy chordae tendineae. Loss of tenomodulin is associated with neoangiogenesis, probably mediated by vascular endothelial growth factor (VEGF)-A. Such changes lead to the degenerative process with matrix metalloproteases (MMPs). The reduced material properties can predispose the chordae for mechanical damage or in the long term for spontaneous rupture.
See this image and copyright information in PMC

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References

    1. Rosamond W, Flegal K, Friday G, Furie K, Go A, Greenlund K, Haase N, Ho M, Howard V, Kissela B, Kittner S, Lloyd-Jones D, McDermott M, Meigs J, Moy C, Nichol G, O’Donnell CJ, Roger V, Rumsfeld J, Sorlie P, Steinberger J, Thom T, Wasserthiel-Smoller S, Hong Y. Heart disease and stroke statistics--2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2007;115:e69–171. - PubMed
    1. Braunwald E. In: Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 6. Braunwald E, Zipes DP, Libby P, editors. Philadelphia, Pa: Saunders Elsevier; 2001. p. 1654.
    1. Millington-Sanders C, Meir A, Lawrence L, Stolinski C. Structure of chordae tendineae in the left ventricle of the human heart. J Anat. 1998;192:573–581. - PMC - PubMed
    1. Kimura N, Shukunami C, Hakuno D, Yoshioka M, Miura S, Docheva D, Kimura T, Okada Y, Matsumura G, Shin’oka T, Yozu R, Kobayashi J, Ishibashi-Ueda H, Hiraki Y, Fukuda K. Local tenomodulin absense, angiogenesis, and MMP activation are associated with the rupture of the chordae tendineae cordis. Circulation. 2008 - PubMed
    1. Pufe T, Petersen WJ, Mentlein R, Tillmann BN. The role of vasculature and angiogenesis for the pathogenesis of degenerative tendons disease. Scand J Med Sci Sports. 2005;15:211–222. - PubMed

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