Key result
Increased myosin regulatory light chain phosphorylation attenuated hypertrophic cardiac responses to voluntary running exercise and isoproterenol treatment in transgenic mice compared to wild-type.
Why the study?
Does increased myosin RLC phosphorylation attenuate cardiac hypertrophy in a mouse model?
Does increased myosin RLC phosphorylation attenuate cardiac hypertrophy in a mouse model?
Increased myosin RLC phosphorylation attenuates rather than causes physiological and pathophysiological cardiac hypertrophy in mice.
No takes yet. Share an insight, caveat, or question.
Should not yet change clinical practice for hypertrophy; hypothesis-generating for myosin RLC phosphorylation in murine stress models.
Huang et al. (2008) studied Cardiac hypertrophy. Overexpression of Ca2+/calmodulin-dependent myosin light chain kinase vs. Wild-type (WT) mice was evaluated on Hypertrophic cardiac responses to voluntary running exercise and isoproterenol treatment. Increased myosin regulatory light chain phosphorylation attenuated hypertrophic cardiac responses to voluntary running exercise and isoproterenol treatment in transgenic mice compared to wild-type.
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