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. Author manuscript; available in PMC: 2020 Mar 1.
Published in final edited form as: Circ Heart Fail. 2019 Mar;12(3):e005529. doi: 10.1161/CIRCHEARTFAILURE.118.005529

Fig. 3.

Fig. 3.

PGC-1α-cKO mice are susceptible to PO-induced heart failure. (A) High mortality rate in PGC-1α-cKO mice under PO conditions. PGC-1α-cKO mice were subjected to TAC. Statistical analysis was performed with the Kaplan-Meier log rank test. (B) Timeline of echocardiography and organ weight measurements. Fractional shortening (FS) (C), lung congestion (D), cardiac hypertrophy (E), PGC-1α target genes expression (F-H), and fatty acid utilization activity (I) were examined in PGC-1α-cKO mice after 2 weeks of TAC. PGC-1α target genes involved in fatty acid metabolism (F), Krebs cycle (G) and mitochondrial ATP production (H). The numbers of mice examined in each experimental group were: 39(Wt)-29(cKO) (A), 7–17(C), 12–26 (D-E), 7–8 (F-H), and 4–9 (I). * p<0.05; ** p<0.01; *** p<0.001 as indicated.