A study using an animal model of myocardial infarction also demonstrated that stellate SGC activation upregulates IL-1β and TNF-α, intensifying cardiac sympathetic hyperinnervation and arrhythmias, while SGC inhibition alleviates the cytokine overdrive and neural overactivity [50], which confirms that SGC targeting could be a viable approach for autonomic dysfunctions akin to those in T2DM. Here, TNF is linked to myocardial infarction.