Key result
S-Propargyl-Cysteine treatment ameliorated myocardial hypertrophy, fibrosis, and cardiac systolic dysfunction in db/db mice through activation of cardiac insulin receptor signaling.
Why the study?
Endogenous hydrogen sulfide is an emerging key signal molecule in diabetic cardiomyopathy, but the effect and underlying mechanism of the novel modulator S-propargyl-cysteine remained to be explored.
Does S-propargyl-cysteine (SPRC) improve diabetic cardiomyopathy in db/db mice?
Population
8-month-old male db/db mice and wild type littermates, and primary neonatal mice cardiomyocytes
Comparison
SPRC vs vehicle
Design
Preclinical in vivo and in vitro laboratory study
Follow-up
12 weeks
Authors
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No immediate clinical implications in diabetic cardiomyopathy; leaves open a role for S-propargyl-cysteine targeting insulin signaling in preclinical models.
Does S-propargyl-cysteine (SPRC) improve diabetic cardiomyopathy in db/db mice?
SPRC attenuates diabetic cardiomyopathy in a mouse model by activating cardiac insulin receptor signaling, suggesting potential therapeutic value for diabetic cardiomyopathy.
Li et al. (2021) studied Diabetic cardiomyopathy. S-Propargyl-Cysteine (SPRC) vs. Vehicle (ddH2O) was evaluated on Myocardial hypertrophy, fibrosis, and cardiac systolic dysfunction. S-Propargyl-Cysteine treatment ameliorated myocardial hypertrophy, fibrosis, and cardiac systolic dysfunction in db/db mice through activation of cardiac insulin receptor signaling.
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