Fig. 8.

Inhibition of ataxia telangiectasia mutated kinase affects the activation of Akt, glycogen synthase kinase (GSK)-3β, AMP-activated protein kinase (AMPK), and mammalian target of rapamycin (mTOR) in cardiac fibroblasts. Serum-starved cardiac fibroblasts were treated with KU-55933 (KU; 100 µm, ataxia telangiectasia mutated kinase inhibitor) for 4 h. Total cell lysates were analyzed by Western blot analysis using anti-phosphorylated (p-)Akt (A), anti-p-GSK-3β (B), anti-p-AMPK (C), and anti-p-mTOR (D) antibodies. A–D, top: Western blots exhibiting immunostaining for p-Akt, p-GSK-3β, p-AMPK, p-mTOR, and GAPDH. A–D, bottom: quantitative analyses of p-Akt, p-GSK-3β, p-AMPK, and p-mTOR normalized to GAPDH. n = 3–4. *P < 0.05 vs. the control (CTL) group.