January 25, 2004American Journal of Hypertension
Mice lacking osteopontin exhibit increased left ventricular dilation and reduced fibrosis after aldosterone infusion
Key result
Osteopontin knockout mice exhibited significantly higher left ventricular end-diastolic diameter and lower fractional shortening (P<.05), along with reduced fibrosis, after aldosterone infusion.
Why the study?
Does osteopontin deficiency alter aldosterone-induced left ventricular remodeling, fibrosis, and apoptosis in mice?
Population
Wild-type and osteopontin knockout mice
Comparison
Aldosterone infusion for up to 4 weeks vs Wild-type mice vs osteopontin knockout mice
Design
Preclinical
Follow-up
4 weeks
Authors
Discussion
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Implication
Osteopontin modulation may have divergent effects on fibrosis versus function; leaves open any therapeutic role in human aldosterone-driven remodeling.
Structured PICO
Does osteopontin deficiency alter aldosterone-induced left ventricular remodeling, fibrosis, and apoptosis in mice?
P
Population
Wild-type and osteopontin knockout mice
I
Intervention
Aldosterone infusion for up to 4 weeks
C
Comparator
Wild-type mice vs osteopontin knockout mice (both receiving aldosterone)
O
Outcome
Left ventricular structural and functional remodeling, fibrosis, and apoptosissurrogate
Main Result
p-value: p=<.05
Osteopontin mediates aldosterone-induced myocardial fibrosis and apoptosis, and its absence exacerbates left ventricular dilation and systolic dysfunction.
Cite This Study
Flora Sam (2004) studied Aldosterone-induced myocardial remodeling. Aldosterone infusion in osteopontin knockout mice vs. Aldosterone infusion in wild-type mice was evaluated on Left ventricular structural and functional remodeling (LV end-diastolic diameter, fractional shortening, fibrosis, apoptosis) (p=<.05). Osteopontin knockout mice exhibited significantly higher left ventricular end-diastolic diameter and lower fractional shortening (P<.05), along with reduced fibrosis, after aldosterone infusion.