Molecular mechanisms of ventricular hypoplasia

D. Srivastava, P. D. Gottlieb, E. N. Olson

Research output: Contribution to journalArticle

6 Scopus citations

Abstract

We have established the beginnings of a road map to understand how ventricular cells become specified, differentiate, and expand into a functional cardiac chamber (Fig. 5). The transcriptional networks described here provide clear evidence that disruption of pathways affecting ventricular growth could be the underlying etiology in a subset of children born with malformation of the right or left ventricle. As we learn details of the precise mechanisms through which the critical factors function, the challenge will lie in devising innovative methods to augment or modify the effects of gene mutations on ventricular development. Because most congenital heart disease likely occurs in a setting of heterozygous, predisposing mutations of one or more genes, modulation of activity of critical pathways in a preventive fashion may be useful in averting disease in genetically susceptible individuals.

Original languageEnglish (US)
Pages (from-to)121-125
Number of pages5
JournalCold Spring Harbor Symposia on Quantitative Biology
Volume67
Publication statusPublished - 2002

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ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Molecular Biology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry

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