Key result
Cardiac-specific overexpression of Tollip significantly attenuated cardiac hypertrophy, fibrosis, and dysfunction in mice subjected to 8 weeks of aortic banding by blocking the AKT signaling pathway.
Population
Cultured neonatal rat cardiomyocytes, transgenic mouse model with cardiac specific-overexpression of Tollip…
Comparison
Tollip overexpression and Tollip… vs Wild-type mice subjected to aortic banding and…
Design
Preclinical
Follow-up
8 weeks
Authors
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May warrant preclinical target validation; leaves open translation to human heart failure.
Tollip serves as a negative regulator of pathological cardiac hypertrophy by blocking the AKT signalling pathway, suggesting a potential therapeutic target for heart failure.
Liu et al. (2013) studied Chronic pressure overload-induced cardiac hypertrophy. Tollip overexpression vs. Wild-type controls was evaluated on Cardiac hypertrophy, fibrosis, and dysfunction. Cardiac-specific overexpression of Tollip significantly attenuated cardiac hypertrophy, fibrosis, and dysfunction in mice subjected to 8 weeks of aortic banding by blocking the AKT signaling pathway.
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