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Despite its clinical importance, a dearth of information exists on the cellular and molecular mechanisms that underpin brain death.One aspect of brain death is cardiovascular deregulation because asystole invariably occurs shortly after its diagnosis.A suitable neural substrate for mechanistic delineation of this aspect of brain death resides in the rostral ventrolateral medulla (RVLM).RVLM is the origin of a life-and-death signal that our laboratory detected from blood pressure of comatose patients that disappears before brain death ensues.At the same time, transcriptional upregulation of heme oxygenase-1 in RVLM by hypoxia-inducible factor-1 (HIF-1) plays a pro-life role in experimental brain death, and HIF-1 is subject to sumoylation activated by transient cerebral ischemia.It follows that sumoylation of HIF-1 in RVLM in response to hypoxia may play a modulatory role on brain stem cardiovascular regulation during experimental brain death.