Key result
Cardiac-specific overexpression of mTOR protected mice against pressure overload-induced cardiac dysfunction and reduced interstitial fibrosis by approximately 60% compared to wild-type controls.
Why the study?
Does mTOR overexpression prevent cardiac dysfunction and attenuate the inflammatory response in pathological hypertrophy?
Population
Transgenic mice with cardiac-specific overexpression of wild-type mTOR and littermate controls subjected to…
Comparison
Cardiac-specific overexpression of wild-type… vs Littermate controls for in vivo; non-transfected…
Design
Preclinical
Follow-up
Up to 4 weeks post-TAC
Authors
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No immediate clinical implications; leaves open mTOR modulation as a therapeutic target in human pressure-overload hypertrophy.
Does mTOR overexpression prevent cardiac dysfunction and attenuate the inflammatory response in pathological hypertrophy?
p-value: p=<0.01
Cardiac-specific overexpression of mTOR protects against pressure overload-induced cardiac dysfunction and fibrosis by attenuating the inflammatory response.
Song et al. (2010) studied Pathological cardiac hypertrophy and heart failure (n=10). Cardiac-specific overexpression of wild-type mTOR vs. Wild-type littermates was evaluated on Interstitial fibrosis and cardiac dysfunction following transverse aortic constriction (p=<0.01). Cardiac-specific overexpression of mTOR protected mice against pressure overload-induced cardiac dysfunction and reduced interstitial fibrosis by approximately 60% compared to wild-type controls.
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