Fig 2: PHB2 overexpression attenuates LPS-induced myocardial depression. WT mice and PHB2 transgenic (PHB2Tg) mice were administered LPS to induce endotoxemia-related myocardial dysfunction. (A-F) Analysis of cardiac function via echocardiography. (G-I) Serum levels of TnT, CK-MB, and BNP were determined by ELISA. (J) Histopathological evaluation of cardiac tissue (HE staining). (K) Electron microscopy (EM) was applied to observe ultrastructural changes in myocardium. Cardiomyocyte swelling, fragmented cardiomyocyte nuclei, and twisted myocardial fibers are marked with red arrows. (L, M) RT-qPCR analysis of the transcription of CXCR7 and TNFα in cardiac tissue. #p<0.05 vs. PBS+WT group; *p<0.05 vs. LPS+WT group.

Fig 3: Pgam5 deletion improves myocardial function in LPS-treated mice. WT mice and cardiomyocyte-specific Pgam5 knockout (Pgam5Cko) mice were administered LPS to induce endotoxemia-related myocardial dysfunction. (A-F) Analysis of cardiac function via echocardiography. (G-I) Serum levels of TnT, CK-MB, and BNP were determined by ELISA. (J) Cardiac histopathology analysis by HE staining. (K) Electron microscopy (EM) was applied to analyze ultrastructural changes in myocardium. Cardiomyocyte swelling, fragmented cardiomyocyte nuclei, and twisted myocardial fibers are marked with red arrows. (L, M) RT-qPCR analysis of CXCR7 and TNFα mRNA levels in heart tissues. #p<0.05 vs. PBS+Pgam5Cko group; *p<0.05 vs. LPS+Pgam5Cko group.

Fig 4: IL-10 and protection from hypertriglyceridemia are necessary for fluoxetine to sustain cardiac glucose oxidation during sepsis.(A and B) U-13C glucose tracing (A) experimental protocol and (B) labeling strategy. (C and D) U-13C glucose labeling of at 7 hours post-infection. (C) Citrate labeling fraction. (D) Pyruvate labeling fraction. n = 7 per condition, one experiment shown. (E) Western blot of pyruvate dehydrogenase (PDH) complex, phospho-PDH, and cyclophilin A of hearts at 8 to 10 hours post-infection. n = 2 to 3 per condition, representative of three independent experiments. (F) Cardiac Pdk4 transcript levels at 10 hours post-infection. n = 5 to 10 per condition, two replicates combined. (G to H) U-13C glucose labeling at 7 hours post-infection of hearts from mice injected with isotype control or anti-IL10R. (G) Citrate labeling fraction. (H) Pyruvate labeling fraction. n = 7 per condition, one experiment shown. (I) Western blot of PDH, phospho-PDH, and cyclophilin A of hearts at 8 to 10 hours post-infection. n = 2 to 3 per condition, representative of two independent experiments. Lower right corner of gel ripped after running. The lower right corner and rest of gel were pieced together for transferring. (J and K) U-13C glucose labeling at 7 hours post-infection in hearts from mice injected with pluronic or water. (J) Citrate labeling fraction. (K) Pyruvate labeling fraction. n = 6 per condition, one experiment shown. (L) Western blot of PDH, phospho-PDH, and cyclophilin A of hearts at 8 to 10 hours post-infection mice injected with water or Pluronic F-127 at the time of infection. n = 2 to 3 per condition, representative of two independent experiments. (M) Circulating BNP levels at 8 to 10 hours post-infection. n = 5 to 15 per condition, three independent experiments combined. (N) Circulating BNP levels at 8 to 10 hours post-infection in mice injected with water or Pluronic. n = 5 to 15 per condition, three independent experiments combined. (O) Model schematic. Two-way ANOVA with Tukey’s multiple comparisons. Uncropped blots are shown in figs. S6 and S7. In all panels, data represent means ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.