Great paper on a new microRNA program that stimulates cardiac regeneration from collaborative work between King's College and Maastricht University.

The miR-106b∼25 cluster, relatively high expressed in the early postnatal myocardium that still retains regenerative potential, directs networks of cell cycle regulators and stimulates proliferation of at least a subset of cardiomyocytes in animal models. In adulthood, the relative low cardiac expression of miR-106b∼25 sustains derepression of prohypertrophic cardiomyocyte gene programs that facilitate adverse remodeling in response to overload. Exploiting this endogenous regulator between cardiomyocyte hyperplasia and hypertrophy by viral gene delivery enhances the endogenous regenerative capacity of the mammalian myocardium and may provide a new therapeutic avenue for the treatment of ischemic heart failure.

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