Modification of Cardiac Phenotype in Tbx1 Hypomorphic Mice

Takatoshi Tsuchihashi; Reina Ishizaki; Jun Maeda; Akimichi Shibata; Keiko Uchida; Deepak Srivastava; Hiroyuki Yamagishi

doi:10.1007/978-4-431-54628-3_28

Modification of Cardiac Phenotype in Tbx1 Hypomorphic Mice

Review

In: Etiology and Morphogenesis of Congenital Heart Disease: From Gene Function and Cellular Interaction to Morphology [Internet]. Tokyo: Springer; 2016. Chapter 28.

2016 Jun 25.

Authors

Takatoshi Tsuchihashi¹, Reina Ishizaki¹, Jun Maeda¹, Akimichi Shibata¹, Keiko Uchida¹, Deepak Srivastava^{2

3}, Hiroyuki Yamagishi¹

Book Editors

Toshio Nakanishi¹, Roger R. Markwald², H.Scott Baldwin³, Bradley B. Keller⁴, Deepak Srivastava⁵, Hiroyuki Yamagishi⁶

Affiliations

¹ Department of Pediatrics, Division of Pediatric Cardiology, Keio University School of Medicine, Tokyo, Japan
² Gladstone Institute of Cardiovascular Disease, San Francisco, CA, 94158, USA
³ Department of Pediatrics and Department of Biochemistry and Biophysics, University of California, San Francisco, San Francisco, CA, 94158, USA

Book Affiliations

¹ Department of Pediatric Cardiology, Tokyo Women's Medical University, Tokyo, Japan
² Cardiovascular Developmental Biology Center, Medical University of South Carolina Clemson University, Charleston, South Carolina, USA
³ Department of Pediatrics (Cardiology), Vanderbilt University, Nashville, Tennessee, USA
⁴ Pediatrics, Pharmacology and Toxicology, and Bioengineering, University of Louisville, Louisville, Kentucky, USA
⁵ Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA
⁶ Pediatrics, Division of Pediatric Cardiology, Keio University School of Medicine, Tokyo, Japan

Excerpt

Congenital heart disease is still the leading cause of death within the first year of life. Our lab forces on understanding the morphology of congenital heart disease. Outflow tract anomalies, including abnormal alignment or septation, account for 30 % of all congenital heart disease. To solve the developmental problem of these defects, we are interested in the role of the second heart field (SHF) that gives rise to the outflow tract structure.

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