Histone H2A.Z Deacetylation and Dedifferentiation in Infarcted/Tip60-depleted Cardiomyocytes.

ABSTRACT: Myocardial infarction (MI) results in the loss of billions of cardiomyocytes (CMs), resulting in cardiac dysfunction. To re-muscularize injured myocardium, new CMs must be generated via renewed proliferation of surviving CMs. Approaches to induce proliferation of CMs after injury have been insufficient. Toward this end we are targeting the acetyltransferase Tip60, encoded by the Kat5 gene, based on the rationale that its pleiotropic functions combine to block CM proliferation at multiple checkpoints. We previously demonstrated that genetic depletion of Tip60 in a mouse model after MI reduces scarring, retains cardiac function, and activates the CM cell-cycle, although it remains unclear whether this culminates in the generation of daughter CMs. In order for pre-existing CMs in the a

SUBMITTER: Wang X 

PROVIDER: S-EPMC10802610 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature