Das D K, Engelman R M, Maulik N
University of Connecticut School of Medicine, Farmington, USA.
Ann N Y Acad Sci. 1999 Jun 30;874:49-65. doi: 10.1111/j.1749-6632.1999.tb09224.x.
This review will focus on the free radical signaling mechanism of preconditioning. The results from our laboratory as well as studies from other laboratories suggest that reactive oxygen species function as second messenger during myocardial adaptation to ischemia. This review provides evidence for the first time that tyrosine kinase and MAP kinases are the targets for reactive oxygen species generated in the preconditioned myocardium. The finding that p38 MAP kinase might be upstream of NF kappa B further supports our previous reports that MAPKAP kinase 2 could be the most likely link between the preconditioning and adaptation mediated by gene expression. p38 activation appears to be an important step in the translocation and activation of the nuclear transcription factor NF kappa B, which in turn may be involved in the induction of the expression of a variety of stress-inducible genes.
本综述将聚焦于预处理的自由基信号传导机制。我们实验室以及其他实验室的研究结果表明，在心肌对缺血的适应性过程中，活性氧作为第二信使发挥作用。本综述首次提供证据表明酪氨酸激酶和丝裂原活化蛋白激酶（MAP激酶）是预处理心肌中产生的活性氧的作用靶点。p38 MAP激酶可能位于核因子κB上游这一发现进一步支持了我们之前的报道，即MAPKAP激酶2可能是预处理与基因表达介导的适应性之间最可能的联系。p38激活似乎是核转录因子NFκB易位和激活的重要步骤，而NFκB反过来可能参与多种应激诱导基因表达的诱导过程。
