Interleukin-1β, Oxidative Stress, and Abnormal Calcium Handling Mediate Diabetic Arrhythmic Risk

•Diabetes-induced arrhythmic risk involved activation of innate immunity, elevation of IL-1β, mitochondrial oxidative stress, SR calcium release channel oxidation, and QT prolongation.•Diabetes-induced arrhythmic risk could be inhibited by IL-1β antagonism, mitoROS scavenging, and SR calcium release stabilization.•The relationship of inflammation and arrhythmic risk may account for increased susceptibility of diabetic patients to the effects of COVID-19.