Key result
Reduced mAKAPβ-SRF phosphorylation in dilated hearts reveals a novel molecular switch and heart failure target.
Why the study?
The molecular mechanisms determining cardiac myocyte preferential growth in width versus length in concentric and eccentric hypertrophy remain poorly understood.
Modulation of the mAKAPβ-SRF signalosome represents a potential new therapeutic target for heart failure by controlling myocyte growth morphology.
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May support mAKAPβ-SRF modulation as a heart failure target; leaves open clinical efficacy pending human trials.
Li et al. (2020) studied Heart failure. AAV-mediated gene delivery / mAKAPβ-SRF signalosome modulation was evaluated on Cardiac myocyte morphology and SRF phosphorylation. Phosphorylation of the mAKAPβ-SRF signalosome is significantly decreased in dilated human hearts, identifying it as a molecular switch controlling myocyte morphology and a target for heart failure.
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