MMP17／MT4-MMP 在胸主动脉瘤发病中的研究进展

• 作 者: 黄吉桢(综述) 王志维(审校)
• 机 构: 430060,武汉大学人民医院心血管外科
• 出 处: 疑难病杂志
• 发表日期: 2016年8期
• 关键词: MMP17/MT4-MMP Thoracic aortic aneurysm VSMC OPN

MMP17／MT4-MMP是膜型基质金属蛋白酶-4，最新研究发现在遗传性胸主动脉瘤患者中存在R373H基因的突变，导致膜型基质金属蛋白酶-4缺乏，骨桥蛋白是新发现的膜型基质金属蛋白酶-4的一种作用底物，缺乏膜型基质金属蛋白酶-4会引起水解产生的氨基端骨桥蛋白减少，进而影响JNK通路调控血管平滑肌细胞的发育，形成不成熟的血管平滑肌细胞，造成主动脉壁正常结构的破坏，在血管紧张素Ⅱ的诱导下形成主动脉瘤的几率增加。这与以往基质金属蛋白酶家族表达增加促进胸主动脉瘤的形成的结论不一致。“,”MMP17/MT4 MMP is membrane type 4 matrix metalloproteinases.The recent research found a missense mutation (R373H) in the inherited thoracic aortic aneurysm(TAA), which would lead to the lack of MMP17/MT4-MMP, the research also showed osteopontin ( OPN) is a new substrate of the MMP17/MT4-MMP.The lack of MMP17/MT4-MMP would lead to the decrease of the N-OPN.N-OPN can regulate the mature of vascular smooth muscle cells by the c-Jun N-terminal kinase ( JNK) signaling.So the lack of MMP17/MT4-MMP would lead to be immature vascular smooth muscle cells and form the incomplete aorta wall, which would increase the susceptibility of thoracic aortic aneurysm.It was not consistent with the previous review that the increase of the MMP family would promote the formation and progression of TAA.