Key result
Tauroursodeoxycholic acid (TUDCA) administration at 300 mg/kg/day significantly attenuated pressure overload-induced cardiac hypertrophy, fibrosis, and apoptosis in mice by reducing endoplasmic reticulum stress.
Why the study?
Does tauroursodeoxycholic acid (TUDCA) attenuate pressure overload-induced cardiac remodeling in a mouse model of transverse aortic constriction?
Population
Male mice aged 8-10 weeks undergoing transverse aortic constriction to induce pressure overload-induced…
Comparison
Tauroursodeoxycholic acid 300 mg/kg/day in water… vs Vehicle administered to TAC-operated mice and…
Design
Preclinical
Follow-up
4 weeks
Authors
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Hypothesis-generating in mouse TAC; leaves open TUDCA translation to human cardiac remodeling.
Does tauroursodeoxycholic acid (TUDCA) attenuate pressure overload-induced cardiac remodeling in a mouse model of transverse aortic constriction?
p-value: p=<0.05
TUDCA attenuates pressure overload-induced cardiac hypertrophy, fibrosis, and apoptosis in mice by reducing endoplasmic reticulum stress, highlighting its potential as a therapeutic agent for maladaptive cardiac remodeling.
Rani et al. (2017) studied Pressure overload-induced cardiac remodeling. Tauroursodeoxycholic acid (TUDCA) vs. Vehicle (water) was evaluated on Cardiac hypertrophy (HW/BW ratio) and endoplasmic reticulum stress markers (p=<0.05). Tauroursodeoxycholic acid (TUDCA) administration at 300 mg/kg/day significantly attenuated pressure overload-induced cardiac hypertrophy, fibrosis, and apoptosis in mice by reducing endoplasmic reticulum stress.
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