Fig. 3
From: Histone lysine dimethyl-demethylase KDM3A controls pathological cardiac hypertrophy and fibrosis
Kdm3a-deficiency protects mice again TAC-induced hypertrophic remodeling. WT and Kdm3a KO (KO) mice were subjected to Sham and TAC surgery. Hearts were echoed and harvested 6 weeks post-surgery for histological and biochemical analysis. a H&E staining of histologic sections of WT and KO mouse hearts. Scale bar, 1 mm. b HW/BW, c relative myocyte size, and d percent of fibrotic area of WT and KO mouse hearts. e LVEDD, f LVESD, g percent FS and heart rate of WT and KO mouse hearts. h Relative mRNA of canonical fetal gene markers (Nppa, Nppb, and Myh7), Fhl1, and Col1a2. mRNA transcripts were measured by qRT-PCR, normalized against internal Gapdh, and expressed relative to Sham WT mice. n = 6-10 ± SEM. *, #p < 0.05 (ANOVA). *, WT TAC vs. WT Sham. #, Tg-TAC vs. WT-TAC
