Why the study?
It is unknown how heterogeneity in fetal-gene re-expression among adult cardiomyocytes is determined and whether differential reprogramming reflects varying degrees of remodeling in pressure-overloaded hearts.
Population
Mice subjected to pressure overload
Comparison
Transverse aortic constriction vs naive controls or glycolysis inhibition with 2-deoxy-d-glucose
Design
Preclinical animal and multiomic study
Follow-up
3 days
Authors
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Identifies early glycolysis as a potential driver of pathological remodeling; leaves open whether targeting this metabolic-.
Early cardiac hypertrophy is characterized by a subpopulation of βMHC-expressing cardiomyocytes with high glycolytic activity that drives pathological remodeling via TEAD1 signaling.
Yeh et al. (2022) studied this question.
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