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A schematic model. In response to pressure overload, MKL1 is recruited to the miR-155 promoter by interacting with NF-κB in macrophages. MKL1 recruitment leads to altered histone modifications and active chromatin remodeling stabilizing NF-κB binding and activating miR-155 transcription. miR-155, likely transmitted via exosomes, acts on the cardiomyocytes to promote hypertrophy.
