Fig. 4: Restoration of PGC1α expression protects against HP-induced mitochondrial energy metabolism dysfunction and cardiac remodeling in both cardiac cells and CKD mice.
From: IRF1-mediated downregulation of PGC1α contributes to cardiorenal syndrome type 4
a–d H9c2 cells were transfected with PGC1α overexpression plasmids or pretreated with Nam, and then treated with control or HP for representative western blot analysis of PGC1α expression (a) ROS production (b) relative mRNA expression of MCAD (FAO), Ndufa (OXPHO), and PFKP (glycolysis) (c), and relative ATP level (d). e Representative gross pathology (HE staining, upper panel. Scale bar, 1 mm) and WGA staining (lower panel. Scale bar, 10 μm) of heart sections from sham, HPD-fed CKD, Nam, and HPD-fed CKD mice intraperitoneally injected with Nam for 12 weeks. n = 10 mice per group. f Cross-sectional surface area of individual cardiac myocytes from the mice in the lower panel of (e). g–j Echocardiography of EF% (g), qPCR analysis of the mRNA expression of hypertrophic genes (h), relative ATP level (i), relative mRNA expression of metabolic genes (j) of heart lysates from the mice in (e). n = 3 (a–d, h, j), or n = 10 (e–g, i). Data are shown as mean ± SD and were analyzed by one-way ANOVA. *P < 0.05, **P < 0.01, ***P < 0.001 versus control or sham. #P < 0.05, ##P < 0.01, ###P < 0.001 versus HP or CKD + HPD.
