Fig. 10

C-Mito^HF exacerbated myocardial remodeling and systolic dysfunction in HF mice through activating endothelial cGAS in the SFO. A Masson staining were performed to assess the myocardial fibrosis in C-Mito^HF-treated HF mice. Scale bar = 150 μm. B Compared to C-Mito^Ctrl, C-Mito^HF exacerbated interstitial and perivascular fibrosis in HF mice, which could be ameliorated by endothelial cGAS KD in the SFO. C WGA staining were performed to assess the cardiomyocyte hypertrophy in C-Mito^HF-treated HF mice. Scale bar = 150 μm. D Compared to C-Mito^Ctrl, C-Mito^HF exacerbated cardiomyocyte hypertrophy in HF mice, which could be ameliorated by endothelial cGAS KD in the SFO. E Echocardiography was conducted to evaluate the cardiac systolic function. Compared to C-Mito^Ctrl, C-Mito^HF significantly decreased the LVEF (F) and LVFS (G) in HF mice, while endothelial cGAS KD in the SFO mitigated the left heart systolic dysfunction in mice. H Lung wet/dry ratio was evaluated in mice. I. Plasmic NT-proBNP level was measured in mice. n = 8, P < 0.05, ANOVA LSD test