2011•Zhongguo bingli shengli zazhiRequires access

Progress in brain protection with ischemic postconditioning

LI Shu-qing

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Abstract

Cerebrocardiovascular diseases and stroke are serious threat to human health.More attentions focus on cerebral ischemia and the publications suggest that ischemic preconditioning prevents ischemic myocardium from ischemia/reperfusion injury,soon followed by preconditioning against cerebral ischemic injury.However,in clinical management,ischemia is often unpredictable.In recent years,researchers found that ischemic postconditioning and ischemic preconditioning obtained the similar effects on brain protection after cerebral ischemia.The endogenous protective mechanisms play a key role in protecting against brain ischemic injury.As a novel manner to protect against brain injury,postconditioning attenuates the infarct volume following brain ischemia/reperfusion and prompts the neurological recovery by prolonging the therapeutic time window.This article reviews the processes of ischemic,hypoxia,hypothermia and pharmacologic postconditioning,and the possible brain protection mechanisms activated by the signal transduction of serine/threonine kinase(Akt),phosphatidylinositol 3-kinase(PI3K),mitogen-activated protein kinase(MAPK),protein kinase C(PKC),and ATP-sensitive potassium channel(KATP) pathways.

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What this paper is about

Cerebrocardiovascular diseases and stroke are serious threat to human health.More attentions focus on cerebral ischemia and the publications suggest that ischemic preconditioning prevents ischemic myocardium from ischemia/reperfusion injury,soon followed by preconditioning against cerebral ischemic injury.However,in clinical management,ischemia is often unpredictable.In recent years,researchers found that ischemic postconditioning and ischemic preconditioning obtained the similar effects on brain protection after cerebral ischemia.The endogenous protective mechanisms play a key role in protecting against brain ischemic injury.As a novel manner to protect against brain injury,postconditioning attenuates the infarct volume following brain ischemia/reperfusion and prompts the neurological recovery by prolonging the therapeutic time window.This article reviews the processes of ischemic,hypoxia,hypothermia and pharmacologic postconditioning,and the possible brain protection mechanisms activated by the signal transduction of serine/threonine kinase(Akt),phosphatidylinositol 3-kinase(PI3K),mitogen-activated protein kinase(MAPK),protein kinase C(PKC),and ATP-sensitive potassium channel(KATP) pathways.

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Available abstract

Cerebrocardiovascular diseases and stroke are serious threat to human health.More attentions focus on cerebral ischemia and the publications suggest that ischemic preconditioning prevents ischemic myocardium from ischemia/reperfusion injury,soon followed by preconditioning against cerebral ischemic injury.However,in clinical management,ischemia is often unpredictable.In recent years,researchers found that ischemic postconditioning and ischemic preconditioning obtained the similar effects on brain protection after cerebral ischemia.The endogenous protective mechanisms play a key role in protecting against brain ischemic injury.As a novel manner to protect against brain injury,postconditioning attenuates the infarct volume following brain ischemia/reperfusion and prompts the neurological recovery by prolonging the therapeutic time window.This article reviews the processes of ischemic,hypoxia,hypothermia and pharmacologic postconditioning,and the possible brain protection mechanisms activated by the signal transduction of serine/threonine kinase(Akt),phosphatidylinositol 3-kinase(PI3K),mitogen-activated protein kinase(MAPK),protein kinase C(PKC),and ATP-sensitive potassium channel(KATP) pathways.

Key concepts: Medicine, Ischemia, Ischemic preconditioning, Protein kinase B, Reperfusion injury, Hypothermia, Brain ischemia, Stroke (engine)

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