Raloxifene Prevents Cardiac Hypertrophy and Dysfunction in Pressure-Overloaded Mice
Key result
Raloxifene prevented increases in left ventricular mass and decreases in fractional shortening in pressure-overloaded mice, and inhibited angiotensin II-induced cardiomyocyte protein synthesis.
Why the study?
Does raloxifene prevent cardiac hypertrophy and dysfunction in pressure-overloaded mice?
Population
Transverse aortic-banded mice and neonatal rat ventricular cardiomyocytes
Comparison
Raloxifene vs Control (no raloxifene)
Design
Preclinical
Follow-up
4 weeks
Authors
Discussion
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Member takes
Implication
No immediate clinical implications; extends preclinical evidence for SERMs in pressure-overload remodeling.
Structured PICO
Does raloxifene prevent cardiac hypertrophy and dysfunction in pressure-overloaded mice?
P
Population
Transverse aortic-banded mice and neonatal rat ventricular cardiomyocytes used to investigate the effects of raloxifene on cardiac hypertrophy.
I
Intervention
Raloxifene
C
Comparator
Control (no raloxifene)
O
Outcome
Left ventricular mass and fractional shortening (in vivo); protein synthesis and MAP kinase phosphorylation (in vitro)surrogate
Raloxifene prevents cardiac hypertrophy and dysfunction in a mouse model of pressure overload, suggesting a potential therapeutic role for selective estrogen receptor modulators in pathological cardiac remodeling.
Cite This Study
Ogita et al. (2003) studied Pressure-overload cardiac hypertrophy. Raloxifene vs. Control / Angiotensin II stimulation without raloxifene was evaluated on Left ventricular mass, fractional shortening, and protein synthesis. Raloxifene prevented increases in left ventricular mass and decreases in fractional shortening in pressure-overloaded mice, and inhibited angiotensin II-induced cardiomyocyte protein synthesis.