Fig. 5

MYH1G-AS modulates skeletal muscle metabolism to activate fast-twitch muscle phenotype and induces muscle atrophy. A−D Relative MYH1G-AS expression (A), relative mtDNA content (B), mitochondrial membrane potential (C), and intracellular ROS ([ROS]i) (D) in gastrocnemius with MYH1G-AS knockdown. E HCA of metabolites in gastrocnemius after infected with Chol-ASO-MYH1G-AS or Chol-ASO-NC. The colors indicate the relative levels in control or MYH1G-AS knockdown group. F Relative metabolite content in MYH1G-AS knockdown gastrocnemius detected by central carbon metabolic profiling. G−N Relative glycogen content (G), IHC analysis (H), MYH1A/MYH7B protein content (I), frequency distribution of MYH1A⁺ (J) and MYH7B⁺ (K) myofiber CSA, relative protein expression of MYH1A and MYH7B (L), relative mRNA expression of several fast- and slow-twitch myofiber genes (M), relative enzymes activity of LDH and SDH (N), relative gastrocnemius muscle weight (O), H&E staining (P), and frequency distribution of fiber CSA (Q) in gastrocnemius with MYH1G-AS knockdown. R Relative mRNA expression of FBXO25 after MYH1G-AS interference detected by RNA-seq. S, T Relative mRNA (S) and protein (T) expression of FBXO25 after MYH1G-AS knockdown. In panel L and T, the numbers shown below the bands were folds of band intensities relative to control. Band intensities were quantified by ImageJ and normalized to β-tubulin. Results are shown as mean ± SEM. In panels A−D, F, G, I, M−O, and R, S), the statistical significance of the differences between means was assessed using paired t-tests. (*P < 0.05; **P < 0.01)