期刊
ANALYSIS OF CARDIAC DEVELOPMENT: FROM EMBRYO TO OLD AGE
卷 1188, 期 -, 页码 177-183出版社
WILEY-BLACKWELL
DOI: 10.1111/j.1749-6632.2009.05098.x
关键词
valvulogenesis; differentiation; mitral valves; periostin; cardiomyopathy; EMT; stem cells
资金
- NIH-NHLBI [HL33756]
- NIH-NCRR [COBRE P20RR016434-07]
- National Science Foundation [FIBRE EF0526854]
- Foundation Leducq (Paris, France) [07CVD04]
- SC INBRE [5MO1RR001070-28]
- American Heart Association [0765280U]
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR016434, M01RR001070] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R37HL033756, R01HL033756, K24HL067434] Funding Source: NIH RePORTER
In this chapter, we review the working hypothesis that the roots of adult valvular heart disease (VHD) lie in embryonic development. Valvulogenesis is a complex process in which growth factors signal the process of endocardium-to-mesenchyme transformation (EMT) resulting in formation of prevalvular cushions. The post-EMT processes, whereby cushions are morphogenetically remolded into valve leaflets, are less well understood, but they require periostin. Mice with targeted deletion of periostin develop degenerative changes similar to human forms of VHD. Mitral valves are also abnormally elongated in hypertrophic cardiomyopathy (HCM), which plays an important role in clinical disease expression. However, the mechanism for this is unclear, but correlates with enhanced expression of periostin in a specific population of ventricular cells derived from the embryonic proepicardial organ, which accumulate at sites where valvular endocardial EMT is reactivated. Collectively, these findings suggest that developmental mechanisms underlie adult valve responses to genetic mutations in degenerative VHD and HCM.
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