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Inducible re-expression of HEXIM1 causes physiological cardiac hypertrophy in the adult mouse

Monica M. Montano, Candida L. Desjardins, Yong Qui Doughman, Yee-Hsee Hsieh, Yanduan Hu, Heather M. Bensinger, Connie Wang, Julian E. Stelzer, Thomas E. Dick, Brian D. Hoit, Margaret P. Chandler, Xin Yu, Michiko Watanabe
DOI: http://dx.doi.org/10.1093/cvr/cvt086 cvt086 First published online: 11 April 2013


Aims The transcription factor hexamethylene-bis-acetamide-inducible protein 1 (HEXIM1) regulates myocardial vascularization and growth during cardiogenesis. Our aim was to determine whether HEXIM1 also has a beneficial role in modulating vascularization, myocardial growth, and function within the adult heart.

Methods and results To achieve our objective, we created and investigated a mouse line wherein HEXIM1 was re-expressed in adult cardiomyocytes to levels found in the foetal heart. Our findings support a beneficial role for HEXIM1 through increased vascularization, myocardial growth, and increased ejection fraction within the adult heart. HEXIM1 re-expression induces angiogenesis, that is, essential for physiological hypertrophy and maintenance of cardiac function. The ability of HEXIM1 to co-ordinate processes associated with physiological hypertrophy may be attributed to HEXIM1 regulation of other transcription factors (HIF-1-α, c-Myc, GATA4, and PPAR-α) that, in turn, control many genes involved in myocardial vascularization, growth, and metabolism. Moreover, the mechanism for HEXIM1-induced physiological hypertrophy appears to be distinct from that involving the PI3K/AKT pathway.

Conclusion HEXIM1 re-expression results in the induction of angiogenesis that allows for the co-ordination of tissue growth and angiogenesis during physiological hypertrophy.

  • HEXIM1
  • Hypertrophy
  • Angiogenesis
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