Circulating mitochondria promoted endothelial cGAS-derived neuroinflammation in subfornical organ to aggravate sympathetic overdrive in heart failure mice, Journal of Neuroinflammation

Figure S2. Experimental microglia depletion by PLX3397 (intragastric

Tumor cells killed by ultrasound-responsive chemotherapeutics triggered

Frontiers Microglia-mediated inflammatory destruction of neuro- cardiovascular dysfunction after stroke

ALDH2 contributes to melatonin-induced protection against APP/PS1 mutation-prompted cardiac anomalies through cGAS-STING-TBK1-mediated regulation of mitophagy

Fragmented mitochondria released from microglia trigger A1 astrocytic response and propagate inflammatory neurodegeneration

Renin-angiotensin system influence on blood pressure. ACE; Angiotensin

IJMS, Free Full-Text

The experimental flow chart of the study.

LCSAA attenuated AMI‐induced astrocyte and neuronal activation in the

Circulating mitochondria promoted endothelial cGAS-derived neuroinflammation in subfornical organ to aggravate sympathetic overdrive in heart failure mice, Journal of Neuroinflammation

Circulating mitochondria promoted endothelial cGAS-derived neuroinflammation in subfornical organ to aggravate sympathetic overdrive in heart failure mice, Journal of Neuroinflammation

Macrophages induce cardiomyocyte ferroptosis via mitochondrial transfer - ScienceDirect

Ultrasound-responsive low-dose doxorubicin liposomes trigger mitochondrial DNA release and activate cGAS-STING-mediated antitumour immunity