Key result
Abrogation of S100B expression in knockout mice augmented hypertrophy, decreased apoptosis, and preserved cardiac function 35 days after experimental myocardial infarction compared to wild-type mice.
Why the study?
Does S100B expression modulate left ventricular remodeling after myocardial infarction in mice?
Does S100B expression modulate left ventricular remodeling after myocardial infarction in mice?
S100B acts as a negative regulator of myocardial hypertrophy after infarction, and its abrogation preserves cardiac function, highlighting it as a potential therapeutic target for post-MI remodeling.
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S100B inhibition may attenuate post-MI remodeling in mice; leaves open whether targeting improves human outcomes.
Tsoporis et al. (2005) studied Myocardial infarction (n=121). S100B genetic modification (knockout or overexpression) vs. Wild-type and sham-operated controls was evaluated on Hypertrophic response, apoptosis, and cardiac function. Abrogation of S100B expression in knockout mice augmented hypertrophy, decreased apoptosis, and preserved cardiac function 35 days after experimental myocardial infarction compared to wild-type mice.
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