Loss of kdm5b ameliorates pathological cardiac fibrosis and dysfunction by epigenetically enhancing atf3 expression

HIGHLIGHTS

• who: Bo Wang from the Mice Wild-type C BL/, mice were obtained from Sipper BK Laboratory Animals (Shanghai, China)KDM, knockout (KO) mice were generated by using the CRISPR/Cas, system. The , bases containing the JmjC domain, which is responsible for its demethylase activity, were deleted from the Kdm5b gene, resulting in a frameshift in the Kdm5b gene and the loss of function of KDM B. All mice were maintained under specific pathogen-free level barrier conditions in the Experimental Animal Center of Tongji University, and all experiments were performed in accordance with procedures approved by . . .
  

   

  

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