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. 2021 Feb 6;47:101185. doi: 10.1016/j.molmet.2021.101185

Figure 6.

Figure 6

Pharmacologic inhibition of EGFR signaling partially restored markers of muscle dysfunction in the M-UVRAG−/−mice. (A) Representative immunoblots (left) and quantification (right) of phospho- and total-Stat3 in quadriceps following oral gavage with vehicle or EGFR inhibitor gefitinib for 21 days (n = 3, each group). (B and C) Relative expression of genes related to muscle dysfunction including Fgf21, Gdf15, and MyoD and mitochondrial function including Mcad, Acox, and Uqcrb in tibialis anterior from the M-UVRAG−/− mice relative to the M-UVRAG+/+ mice after treatment with vehicle or gefitinib for 21 days (n = 3, each group). Data shown are mean ± S.E.M. ∗p < 0.05, ∗∗p < 0.01 and ∗∗∗p < 0.001 using Student's t test.