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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, RESULTS. Meshes: Animals, Cells, Cultured, DNA, Mitochondrial, Gene Silencing, Hemodynamics, Hypertrophy, Left Ventricular, Intracellular Signaling Peptides and Proteins, MEF2 Transcription Factors, Mice, Myocardium, Myocytes, Cardiac, Myogenic Regulatory Factors, Protein-Serine-Threonine Kinases, RNA, Small Interfering, Rats, Ribosomal Protein S6 Kinases, 90-kDa, Signal Transduction, TOR Serine-Threonine Kinases, Ventricular Pressure.
user
Does mEF2C silencing attenuate load-induced left ventricular hypertrophy by modulating mTOR/S6K pathway in mice? Context: The activation of the members of the myocyte enhancer factor-2 family (MEF2A, B, C and D) of transcription factors promotes cardiac hypertrophy and failure. However, the role of its individual components in the pathogenesis of cardiac hypertrophy remains unclear. In this study, we investigated whether MEF2C plays a role in mediating the left ventricular hypertrophy by pressure overload in mice. The knockdown of myocardial MEF2C induced by specific small interfering RNA (siRNA) has been shown to attenuate hypertrophy, interstitial fibrosis and the rise of ANP levels in aortic banded mice. We detected that the depletion of MEF2C also results in lowered levels of both PGC-1alpha and mitochondrial DNA in the overloaded left ventricle, associated with enhanced AMP:ATP ratio. Additionally, MEF2C depletion was accompanied by defective activation of S6K in response to pressure overload. Treatment with the amino acid leucine stimulated S6K and suppressed the attenuation of left ventricular hypertrophy and fibrosis in the aforementioned aortic banded mice.
assistant
These findings represent new evidences that MEF2C depletion attenuates the hypertrophic responses to mechanical stress and highlight the potential of MEF2C to be a target for new therapies to cardiac hypertrophy and failure. Final Decision: yes