Adaptive mechanisms that preserve cardiac function in mice without myoglobin

A. P. Meeson, N. Radford, J. M. Shelton, P. P.A. Mammen, J. M. DiMaio, K. Hutcheson, Y. Kong, J. Elterman, R. S. Williams, D. J. Garry

Research output: Contribution to journalArticlepeer-review

75 Scopus citations


Mice lacking myoglobin survive to adulthood and meet the circulatory demands of exercise and pregnancy without cardiac decompensation. In the present study, we show that many myoglobin-deficient embryos die in utero at midgestation with signs of cardiac failure. Fetal mice that survive to gestational day 12.5, however, suffer no subsequent excess mortality. Survival in the absence of myoglobin is associated with increased vascularity and the induction of genes encoding the hypoxia-inducible transcription factors 1 α and 2, stress proteins such as heat shock protein 27, and vascular endothelial growth factor. These adaptations are evident in late fetal life, persist into adulthood, and are sufficient to maintain normal myocardial oxygen consumption during stressed conditions. These data reveal that myoglobin is necessary to support cardiac function during development, but adaptive responses evoked in some animals can fully compensate for the defect in cellular oxygen transport resulting from the loss of myoglobin.

Original languageEnglish (US)
Pages (from-to)713-720
Number of pages8
JournalCirculation research
Issue number7
StatePublished - Apr 13 2001


  • Hypoxia
  • Metabolism
  • Myoglobin
  • Transgenic mice
  • Vasculature


Dive into the research topics of 'Adaptive mechanisms that preserve cardiac function in mice without myoglobin'. Together they form a unique fingerprint.

Cite this