PDP1 and cardiac arrest: Inhibition of PDK4 can reduce succinic acid accumulation and inhibit ROS-induced nephrotoxicity.[95] Animal model studies have demonstrated that DCA inhibits PDK, increases PDH activity, and enhances hemodynamics and prognosis following cardiac arrest.[96,97] Enhanced PDH activity by DCA alleviated cardiac systolic dysfunction after ischemia-induced ventricular fibrillation.[98] These studies suggest that single-dose DCA may be valuable in acute critical situations and avoid peripheral neurotoxicity associated with long-term use.