JNK1/2信号通路介导低剪切力促穿支皮瓣choke血管增生机制研究

The methods to expand the blood supply of perforator flap have been the focus of both basic and clinical research, with the effective measures still being sought. Choke vessels is the key structure of the blood flow among the perforasome in a perforator flap. However, the current studies are limited to the morphology of choke vessels, not the function or the mechanism of regulation. Different from collateral vessels, hemodynamics change includes high blood pressure，high resistance and low shear force，as is evidenced in our previous research. This kind of hemodynamics change promotes choke vessels angiogenesis, which is closely relative to JNK1/2 signaling pathway. No study is conducted in this field. Therefore, based on the three steps of choke vessels angiogenesis, our study consists of the mechanism of low shear force activating the JNK1/2 signaling pathway, the mechanism of JNK1/2 signaling pathway promoting choke vessels angiogenesis and the mechanism of cytokine promoting choke vessels angiogenesis by JNK1/2 signaling pathway. A new method will be established to expand the blood supply of perforator flap if the assumption is been realized.

如何拓展穿支皮瓣的血供历来是基础与临床研究的重点，但一直缺乏有效的措施。我们发现：闭塞血管是穿支皮瓣穿支体之间血供扩散的关键结构，但国内外目前的研究局限于闭塞血管形态学研究，未从功能及调控路径上进行探讨。我们前期研究显示穿支皮瓣形成后，不同于侧枝血管，闭塞血管的血流动力学改变为高血流压力、高阻力及血流剪切力降低。该血流动力学的改变促使闭塞血管增生，而血管增生的传导途径与JNK1/2信号通路密切相关，但缺乏相关研究。因此，在总结闭塞血管增生的三步骤基础上，本课题研究（1）低剪切力激活并调控JNK1/2信号通路的机制；（2）低剪切力通过JNK1/2信号通路的激活促choke血管增生的机制；（3）常见促血管增生细胞因子通过JNK1/2通路增强低剪切力促choke血管增生效率的机制。如果本课题的设想得以验证，将为调控穿支皮瓣血供开辟新的思路。

拓展穿支皮瓣的血供一直缺乏有效的措施，choke血管是穿支皮瓣穿支体之间血供扩散的关键结构，因此，choke血管成为基础与临床研究的重点。本研究从choke血管形态学研究及功能及调控路径上进行研究探讨。本课题证实并验证了：（1）低剪切力激活并调控JNK1/2信号通路的机制；（2）低剪切力通过JNK1/2信号通路的激活促choke血管增生的机制；（3）常见促血管增生细胞因子通过JNK1/2通路增强低剪切力促choke血管增生效率的机制。在该领域未见类似报道，并为调控穿支皮瓣血供开辟新的思路，同时，发现choke血管有不同类型并有不同的增生因素，如缺氧、张力及剪切力，是未来研究方向。将本课题研究成果已发表论文2篇，同时有两篇论文已完成书写并投稿。本课题成果也获得国内论文比赛二等奖，并作为课题组其它成员国自课题的前期工作基础。