Figure 6

The possible process through which HHS modifies Cx43 and causes arrhythmia is depicted in a cartoon. By triggering the HPA axis, HHS raises blood glucose levels and suppresses the activity of LKB1. This, in turn, hampers the expression of AMPK, or HHS directly inhibits AMPK expression. Ultimately, these mechanisms contribute to the development of arrhythmias by further influencing the remodeling of Cx43 and initiating fibrosis after inflammatory responses.