Key result
Cardiomyocyte-specific overexpression of RGS2eb inhibited cardiac hypertrophy and improved cardiac function in mice following 4 weeks of transverse aortic constriction compared to wild-type controls.
Why the study?
Does cardiomyocyte specific overexpression of RGS2eb inhibit cardiac hypertrophy and improve function in mice subjected to pressure overload?
Population
Mice subjected to transverse aortic constriction (TAC) in a pressure-overload hypertrophy model
Comparison
Cardiomyocyte specific overexpression of a 37… vs Wild-type (WT) controls
Design
Preclinical
Follow-up
4 weeks
Authors
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Preclinical finding only; leaves open whether RGS2eb modulation can treat human pressure-overload cardiomyopathy.
Does cardiomyocyte specific overexpression of RGS2eb inhibit cardiac hypertrophy and improve function in mice subjected to pressure overload?
Cardiomyocyte-specific overexpression of the RGS2eb domain limits pathological cardiac hypertrophy and improves cardiac function in a mouse model of pressure overload.
Lee et al. (2017) studied Cardiac hypertrophy. Cardiomyocyte specific overexpression of RGS2eb vs. Wild-type (WT) controls was evaluated on Cardiac hypertrophy and cardiac function following transverse aortic constriction (TAC). Cardiomyocyte-specific overexpression of RGS2eb inhibited cardiac hypertrophy and improved cardiac function in mice following 4 weeks of transverse aortic constriction compared to wild-type controls.
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