Based on our results, UCP2 appears to play an important role in the high-salt diet-dependent increased susceptibility to cerebrovascular events, as well as it does for the increased susceptibility to kidney damage of SHRSP.23, 24, 25 A common molecular mechanism, dependent on UCP2 suppression, may underlie the vascular damage observed in different organs of high-salt-fed SHRSP. Here, UCP2 is linked to Nephropathy.