Fig. 8From: Circulating mitochondria promoted endothelial cGAS-derived neuroinflammation in subfornical organ to aggravate sympathetic overdrive in heart failure miceC-MitoHF increased cardiac sympathetic hyperactivation depending on the SFO endothelial cGAS in HF mice. A Renal sympathetic activity (RSNA) of mice were evaluated to determine the cardiovascular sympathetic output in C-MitoHF-treated HF mice. B Compared to C-MitoCtrl, C-MitoHF significantly increased the RSNA level in HF mice, while endothelial cGAS KD in the SFO ameliorated the sympathoexcitation effect of C-MitoHF in HF mice. C The results of heart rate variability (HRV) analysis showed C-MitoHF decreased LF/HF ratio of HF mice, which implies cardiac sympathetic/parasympathetic tones imbalance with the sympathetic overactivation, while endothelial cGAS KD in the SFO ameliorated this effect. n = 8, P < 0.05, ANOVA LSD testBack to article page