期刊
AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS
卷 163, 期 3, 页码 157-168出版社
WILEY
DOI: 10.1002/ajmg.c.31366
关键词
cardiac chamber maturation; cardiac trabeculation; conduction; cardiomyocyte proliferation; Left Ventricular Non-Compaction (LVNC); Neuregulin; Notch; Ephrin; BMP; Semaphorin; FGF; Retinoic acid; endothelin; extracellular matrix signaling
资金
- NHLBI [HL109079]
- University of North Carolina, Chapel Hill
Congenital heart diseases are some of the most common human birth defects. Though some congenital heart defects can be surgically corrected, treatment options for other congenital heart diseases are very limited. In many congenital heart diseases, genetic defects lead to impaired embryonic heart development or growth. One of the key development processes in cardiac development is chamber maturation, and alterations in this maturation process can manifest as a variety of congenital defects including non-compaction, systolic dysfunction, diastolic dysfunction, and arrhythmia. During development, to meet the increasing metabolic demands of the developing embryo, the myocardial wall undergoes extensive remodeling characterized by the formation of muscular luminal protrusions called cardiac trabeculae, increased cardiomyocyte mass, and development of the ventricular conduction system. Though the basic morphological and cytological changes involved in early heart development are clear, much remains unknown about the complex biomolecular mechanisms governing chamber maturation. In this review, we highlight evidence suggesting that a wide variety of basic signaling pathways and biomechanical forces are involved in cardiac wall maturation. (c) 2013 Wiley Periodicals, Inc.
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