Telomerase reverse transcriptase: a novel neuroprotective mechanism involved in neonatal hypoxic-ischemic brain injury

Abstract

Hypoxic-ischemic (HI) brain injury is one of the most severe diseases in the neonatal central nervous system (CNS). The pathological mechanisms of HI brain injury, including cellular apoptosis, excitotoxicity, oxidative stress, etc., are complicated and not well known. Cellular processes such as angiogenesis, neuronal survival and neurogenesis have been proven to be closely associated with brain repair following HI injury. Telomerase reverse transcriptase (TERT), a component of telomerase, plays a primary role in maintaining telomere length. In addition, recent studies have demonstrated that TERT can protect neurons from apoptosis and excitotoxicity, and promote angiogenesis, neurogenesis and neuronal survival. However, there are few reports on the roles of TERT in neonatal HI brain injury and the mechanisms involved are unclear. It is reported that TERT is activated and plays a protective role in adult brains with ischemia and recently we have shown that TERT was induced and may act protectively in a neonatal rat model of HI brain injury. Therefore, it is quite possible that TERT plays an important role in neuroprotection in developing brains following HI injury by inhibiting apoptosis and excitotoxicity, and promoting angiogenesis, neuronal survival and neurogenesis. These very novel mechanisms could lead to more effective neuroprotective strategies against hypoxic-ischemic brain injury in neonates.