November 1, 2013Current Pharmaceutical Design
The STAT3 Inhibitor Stattic Impairs Cardiomyocyte Mitochondrial Function Through Increased Reactive Oxygen Species Formation
Key result
Inhibition of mitochondrial STAT3 by 100 µM Stattic increased ROS formation compared to control (9.23 vs 0.39, p<0.05), which impaired ATP production and enhanced MPTP opening.
Population
Isolated rat left ventricular mitochondria
Comparison
Stattic at doses of 1, 10, 25, 50, and 100 µM… vs Control mitochondria (DMSO)
Design
Preclinical
Authors
Discussion
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Implication
Mitochondrial STAT3 inhibition disrupts rat cardiomyocyte energetics; leaves open its relevance as a therapeutic target in human cardiac disease.
Structured PICO
P
Population
Isolated rat left ventricular mitochondria preparations used to evaluate the effects of the STAT3 inhibitor Stattic.
I
Intervention
Stattic (STAT3-specific inhibitor) at doses of 1, 10, 25, 50, and 100 µM, with or without N-acetylcysteine (Nac)
C
Comparator
Control mitochondria (DMSO)
O
Outcome
Mitochondrial reactive oxygen species (H2O2) formationsurrogate
Main Result
Absolute Event Rate: 9.23% vs 0.39%
p-value: p=<0.05
Inhibition of mitochondrial STAT3 by Stattic impairs mitochondrial ATP production and enhances MPTP opening through increased reactive oxygen species formation in isolated rat cardiomyocytes.
Cite This Study
Boengler et al. (2013) studied this question. Stattic vs. DMSO (control) was evaluated on Mitochondrial ROS formation (slope of Amplex UltraRed fluorescence/time) (p=<0.05). Inhibition of mitochondrial STAT3 by 100 µM Stattic increased ROS formation compared to control (9.23 vs 0.39, p<0.05), which impaired ATP production and enhanced MPTP opening.