1998
DOI: 10.1038/27681
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Abstract: Myoglobin, an intracellular haemoprotein expressed in the heart and oxidative skeletal myofibres of vertebrates, binds molecular oxygen and may facilitate oxygen transport from erythrocytes to mitochondria, thereby maintaining cellular respiration during periods of high physiological demand. Here we show, however, that mice without myoglobin, generated by gene-knockout technology, are fertile and exhibit normal exercise capacity and a normal ventilatory response to low oxygen levels (hypoxia). Heart and soleus… Show more

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Cited by 256 publications
(218 citation statements)
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“…Neither the cardiac nor any infiltrating nonmuscle cells were able to completely compensate for the loss of the cardiomyocyte-derived VEGF, underlining the importance of VEGF and its production in the cardiomyocytes during the development of the myocardial vasculature. In contrast, a myoglobin knockout mouse line has been reported recently in which compensatory increases in the capillary density, hematocrit, coronary flow, and coronary flow reserve were so effective that the myo -/-mice were phenotypically normal (26,27).…”
Section: Discussionmentioning
confidence: 95%
“…Neither the cardiac nor any infiltrating nonmuscle cells were able to completely compensate for the loss of the cardiomyocyte-derived VEGF, underlining the importance of VEGF and its production in the cardiomyocytes during the development of the myocardial vasculature. In contrast, a myoglobin knockout mouse line has been reported recently in which compensatory increases in the capillary density, hematocrit, coronary flow, and coronary flow reserve were so effective that the myo -/-mice were phenotypically normal (26,27).…”
Section: Discussionmentioning
confidence: 95%
“…In contrast, other studies and analyses suggest that Mb may contribute more to the NIRS signal than previously thought, possibly even more than Hb. Due to the potentially significant role of Mb in oxygen transport from capillary to mitochondria (Richardson et al, 2006, Richardson et al, 2001, Groebe and Thews, 1990, Garry et al, 1998) the contribution of Mb to the NIRS signal needs to be re-examined.…”
Section: Statement Of the Problemmentioning
confidence: 99%
“…Knockout mice also demonstrate an increased expression of hypoxia-induced genes coding for vascular endothelial growth factor and nitric oxide synthase. The increased expression of these genes may provide the basis for the cellular adaptations seen in knockout mice (Ordway and Garry, 2004, Garry et al, 1998, Godecke et al, 1999. While these mice are able to function normally without Mb, Mb-facilitated oxygen diffusion may be important in delivering oxygen to the mitochondria.…”
Section: Chapter 1 -Introductionmentioning
confidence: 99%
“…Another, more controversially discussed role is Mbs' facilitation of O 2 diffusion within muscle cells (Wittenberg, 1970;Jürgens et al, 1994). Although Mb knockout mice exhibited normal exercise capacity and no signs of compromised cardiac energetics due to multiple systemic compensations (Garry et al, 1998;Gödecke et al, 1999), follow-up studies stressed the importance of functional Mb in maintaining nitric oxide (NO) homeostasis in muscle through either scavenging (Flögel et al, 2001) or producing the NO molecule (Hendgen-Cotta et al, 2008). That way, Mb might participate in tuning vasodilatory responsiveness and protecting the respiratory chain from NO inhibition (Brunori, 2001).…”
mentioning
confidence: 99%