Wenjun Zhang, M.D. is a research assistant professor of Pediatrics, Riley Heart Research Center, Indiana University School of Medicine. His research focuses on molecular signaling in regulating mammalian heart development and heart failure.
Molecular mechanism of ventricular trabeculation/compaction and the pathogenesis of the left ventricular noncompaction cardiomyopathy (LVNC)†
Article first published online: 10 JUL 2013
Copyright © 2013 Wiley Periodicals, Inc.
American Journal of Medical Genetics Part C: Seminars in Medical Genetics
Special Issue: Disorders of Left Ventricular Trabeculation/Compaction or Right Ventricular Wall Formation
Volume 163, Issue 3, pages 144–156, August 2013
How to Cite
2013. Molecular mechanism of ventricular trabeculation/compaction and the pathogenesis of the left ventricular noncompaction cardiomyopathy (LVNC). Am J Med Genet Part C Semin Med Genet 163C:144–156., , , , .
Conflict of interest: none.
- Issue published online: 23 JUL 2013
- Article first published online: 10 JUL 2013
- National Institute of Health
- Riley Children's Foundation
- American Heart Association Established Investigator Award
- March of Dimes Foundation
- CHARGE Syndrome Foundation
- Oak Foundation
- Stanford Child Health Research Institute
Ventricular trabeculation and compaction are two of the many essential steps for generating a functionally competent ventricular wall. A significant reduction in trabeculation is usually associated with ventricular compact zone deficiencies (hypoplastic wall), which commonly leads to embryonic heart failure and early embryonic lethality. In contrast, hypertrabeculation and lack of ventricular wall compaction (noncompaction) are closely related defects in cardiac embryogenesis associated with left ventricular noncompaction (LVNC), a genetically heterogenous disorder. Here we review recent findings through summarizing several genetically engineered mouse models that have defects in cardiac trabeculation and compaction. © 2013 Wiley Periodicals, Inc.