Key result
Forced expression of S100beta inhibited alpha1-adrenergic and hypoxia-induced hypertrophic gene expression in cultured neonatal rat cardiac myocytes.
S100beta may act as an intrinsic negative regulator of the hypertrophic response in cardiac myocytes post-infarction, potentially limiting adverse ventricular remodeling.
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Hypothesis-generating for fetal gene reprogramming in post-MI hypertrophy; extends beta-MHC observations in rodent models but translation untested.
Tsoporis et al. (1997) studied Myocardial infarction and cardiac hypertrophy. S100beta expression was evaluated on alpha1-adrenergic induction of beta-myosin heavy chain and skeletal alpha-actin promoters. Forced expression of S100beta inhibited alpha1-adrenergic and hypoxia-induced hypertrophic gene expression in cultured neonatal rat cardiac myocytes.
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