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JNK在脑缺血再灌注损伤细胞凋亡中的作用

The Role of JNK in Apoptosis after Cerebral Ischemia-Reperfusion Injury
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摘要 缺血性脑卒中发病率逐年增高,严重威胁人们的健康与生活质量,脑缺血/再灌注损伤(CIRI)是其发病及治疗过程中常见的不良后果之一。c-jun氨基末端激酶(JNK)信号转导通路在CIRI中起着重要的调控作用,参与介导了神经元凋亡等病理生理过程,是防治CIRI的重要靶点。许多研究提示,JNK抑制剂可以减少CIRI引起的细胞凋亡,发挥神经保护作用,可为临床上缺血性脑卒中的治疗提供新的思路,同时对寻找新的药物靶点和筛选新药都具有重要的理论意义。 The incidence rate of ischemic stroke is increasing year by year, which seriously threatens people’s health and quality of life. Cerebral ischemia/reperfusion injury (CIRI) is one of the common adverse consequences in the course of its onset and treatment. C-Jun N-terminal kinase (JNK) signal transduction pathway plays an important role in the regulation of CIRI. It participates in the pathophysiological processes such as neuronal apoptosis, and is an important target for the prevention and treatment of CIRI. Many studies suggest that JNK inhibitors can reduce the apoptosis induced by CIRI and play a neuroprotective role, which can provide a new idea for the treatment of ischemic stroke in clinic. At the same time, it has important theoretical significance for finding new drug targets and screening new drugs.
出处 《临床医学进展》 2021年第5期21111-2119,共9页 Advances in Clinical Medicine
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