Key result
Inhibition of SMAD proteins using decoy or antisense oligonucleotides reduced SNAP-induced apoptosis in rat ventricular cardiomyocytes from 13.3% to control levels of 8% (p<0.05).
Population
Isolated ventricular cardiomyocytes of rat
Comparison
NO donor SNAP or TGFbeta, with or without SMAD… vs Control conditions
Design
Preclinical
Authors
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May support SMAD inhibition to limit cardiomyocyte apoptosis; hypothesis-generating in animal models and requires clinical validation.
Absolute Event Rate: 8% vs 13.3%
p-value: p=< 0.05
SMAD proteins are essential for AP-1-mediated apoptosis but not hypertrophic growth in ventricular cardiomyocytes, suggesting a mechanism for shifting AP-1 signaling in the failing heart.
SCHNEIDERS et al. (2005) studied isolated ventricular cardiomyocytes of rat under hypertrophy- or apoptosis-inducing conditions. SMAD decoy oligonucleotides or SMAD4 antisense oligonucleotides vs. control (SNAP stimulation alone) was evaluated on number of apoptotic cells (p=< 0.05). Inhibition of SMAD proteins using decoy or antisense oligonucleotides reduced SNAP-induced apoptosis in rat ventricular cardiomyocytes from 13.3% to control levels of 8% (p<0.05).
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