SOD1 and diabetes mellitus: Since our data indicate that hSOD1 overexpression did not cause dysfunction of MAP, HR, and BRS but may increase aortic baroreceptor nerve function, we suggest that this model can be potentially used to study whether increased expression of hSOD1 protects against disease (such as chronic intermittent hypoxia and diabetes-) induced impairment of baroreflex sensitivity, vagal motor neuron death in the nucleus ambiguus, and degeneration of vagal afferent and efferent axons in the aortic arch and cardiac ganglion shown in the previous studies [51, 52, 55, 84–86].