支架植入后抑制平滑肌细胞过度增殖的研究进展

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Abstract In-stent restenosis (ISR) is a major complication that limits the efficacy of stent implantation and seriously affects patients′ quality of life. The excessive proliferation of smooth muscle cells at the site of vascular injury is the main reason for the formation of early ISR. Although the advent of drug-coated stents and biodegradable stents has reduced the risk of ISR, late complications are still at a high level, and the applicable materials of biodegradable stents are still in the exploration stage. This article mainly summarizes the related mechanisms and treatment methods of smooth muscle cells in the process of ISR from the aspect of inhibiting the excessive proliferation of smooth muscle cells, hoping to provide ideas for clinical treatment and experimental research.

Key words： In-stent restenosis Vascular smooth muscle cells Research progress

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	HU Zhimin LING Wang WU Meiping

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HU Zhimin LING Wang WU Meiping. Research progress on inhibiting excessive proliferation of smooth muscle cells after stent implantation[J]. 中国医药导报, 2020, 17(7): 27-30.

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http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2020/V17/I7/27

[1] Tesfamariam B. Endothelial Repair and Regeneration Following Intimal Injury [J]. J Cardiovasc Transl Res，2016，9（2）：91-101.
[2] Ke L，Huang Y，Liu L，et al. Bioresorbable Vascular Scaffold：A Focused Review on Development and Preclinical Studies [J]. Zhongguo Yi Liao Qi Xie Za Zhi，2018，42（2）：115-118.
[3] 赵琪，冉峰.药物涂层支架的研究进展[J].中国血管外科杂志：电子版，2017，9（2）：156-160.
[4] Tomaniak M，Ko?覥towski ?覵，Pietrasik A，et al. A serial 3- and 9-year optical coherence tomography assessment of vascular healing response to sirolimus- and paclitaxel-eluting stents [J]. Int J Cardiovasc Imaging，2019，35（1）：9-21.
[5] Harari E，Guo L，Smith SL，et al. Direct Targeting of the mTOR（Mammalian Target of Rapamycin）Kinase Improves Endothelial Permeability in Drug-Eluting Stents [J]. Arterioscler Thromb Vasc Biol，2018，38（9）：2217-2224.
[6] Ma X，Jiang C，Li Y，et al. Inhibition effect of tacrolimus and platelet-derived growth factor-BB on restenosis after vascular intimal injury [J]. Biomed Pharmacother，2017， 93：180-189.
[7] 杜长春.药物洗脱支架与金属支架置入后再狭窄及其生物相容性比较[J].中国组织工程研究与临床康复，2009， 13（39）：7735-7738.
[8] Indolfi C，Iaconetti C，Gareri C，et al. Non-coding RNAs in vascular remodeling and restenosis [J]. Vascul Pharmacol，2019，114：49-63.
[9] 周孜孜.转化生长因子-β_1诱导人主动脉平滑肌细胞表型转化的作用及机制研究[D].广州：南方医科大学，2016.
[10] 杜明昭.载人HGF与TGF-β1-shRNA功能基因涂层血管内支架的实验研究[D].长春：吉林大学，2014.
[11] Tao J，Barnett JV，Watanabe M，et al. Hypoxia Supports Epicardial Cell Differentiation in Vascular Smooth Muscle Cells through the Activation of the TGFβ Pathway [J]. J Cardiovasc Dev Dis，2018，5（2）：19.
[12] 孙岚，辛文妤，于昕，等.非对称性二甲基精氨酸通过Rho/ROCK信号通路介导大鼠血管平滑肌细胞迁移[J].中国分子心脏病学杂志，2012，12（1）：37-42.
[13] Luo X，Liu J，Zhou H，et al. Apelin/APJ system：A critical regulator of vascular smooth muscle cell [J]. J Cell Physiol，2018，233（7）：5180-5188.
[14] 李罗成，王志维，胡知朋，等.Fibulin-2调控的TGF-β/Smad信号通路在VSMCs凋亡中的作用[J].武汉大学学报：医学版，2018，39（3）：380-384.
[15] 蔡松志.miR-206靶向ZFP580调控平滑肌细胞表型转换研究[D].石家庄：河北医科大学，2015.
[16] Dong LH，Wen JK，Miao SB，et al. Baicalin inhibits PDGF-BB-stimulated vascular smooth muscle cell proliferation through suppressing PDGFRβ-ERK signaling and increase in p27 accumulation and prevents injury-induced neointimal hyperplasia [J]. Cell Res，2010，20（11）：1252-1262.
[17] Zhang Q，Chen L，Zhao Z，et al. HMGA1 Mediated High-Glucose-Induced Vascular Smooth Muscle Cell Proliferation in Diabetes Mellitus：Association Between PI3K/Akt Signaling and HMGA1 Expression [J]. DNA Cell Biol，2018，37（4）：389-397.
[18] Sun L，Zhao M，Liu A，et al. Shear Stress Induces Phenotypic Modulation of Vascular Smooth Muscle Cells via AMPK/mTOR/ULK1-Mediated Autophagy [J]. Cell Mol Neurobiol，2018，38（2）：541-548.
[19] Tan P，Wang YJ，Li S，et al. The PI3K/Akt/mTOR pathway regulates the replicative senescence of human VSMCs [J]. Mol Cell Biochem，2016，422（1/2）：1-10.
[20] Yan H，Peng X，Xu H，et al. Inhibition of Aortic Intimal Hyperplasia and Vascular Smooth Muscle Proliferation and Extracellular Matrix Protein Expressions by Astragalus-Angelica Combination [J]. Evid Based Complement Alternat Med，2018，2018：1-15.
[21] Doronzo G，Viretto M，Russo I，et al. Nitric oxide activates PI3-K and MAPK signalling pathways in human and rat vascular smooth muscle cells：influence of insulin resistance and oxidative stress [J]. Atherosclerosis，2011， 216（1）：44-53.
[22] Yang Z，Yang Y，Zhang L，et al. Mussel-inspired catalytic selenocystamine-dopamine coatings for long-term generation of therapeutic gas on cardiovascular stents [J]. Biomaterials，2018，178：1-10.
[23] Liao XH，Xiang Y，Li H，et al. VEGF-A Stimulates STAT3 Activity via Nitrosylation of Myocardin to Regulate the Expression of Vascular Smooth Muscle Cell Differentiation Markers [J]. Sci Rep，2017，7（1）：2660.
[24] Gareri C，Iaconetti C，Sorrentino S，et al. miR-125a-5p Modulates Phenotypic Switch of Vascular Smooth Muscle Cells by Targeting ETS-1 [J]. J Mol Biol，2017，429（12）：1817-1828.
[25] Kadam AA，Gersch RP，Rosengart TK，et al. Inflammatory monocyte response due to altered wall shear stress in an isolated femoral artery model [J]. J Biol Methods，2019，6（1）：e109.
[26] Hasan RN，Schafer AI. Hemin upregulates Egr-1 expression in vascular smooth muscle cells via reactive oxygen species ERK-1/2-Elk-1 and NF-kappaB [J]. Circ Res，2008，102（1）：42-50.
[27] Simo-Cheyou ER，Tan JJ，Grygorczyk R，et al. STIM-1 and ORAI-1 channel mediate angiotensin-Ⅱ-induced expression of Egr-1 in vascular smooth muscle cells [J]. J Cell Physiol，2017，232（12）：3496-3509.
[28] Chen W，Xiao L，Bai J，et al. The promotion of tissue engineering blood vessel patency by CGS21680 through regulating pro-inflammatory activities of endothelial progenitor cell [J]. J Biomed Mater Res A，2018，106（10）：2634-2642.
[29] Zhang Y，You B，Liu X，et al. High-Mobility Group Box 1（HMGB1）Induces Migration of Endothelial Progenitor Cell via Receptor for Advanced Glycation End-Products （RAGE）-Dependent PI3K/Akt/eNOS Signaling Pathway [J]. Med Sci Monit，2019，25：6462-6473.
[30] Chang HK，Kim PH，Kim DW，et al. Coronary stents with inducible VEGF/HGF-secreting UCB-MSCs reduced restenosis and increased re-endothelialization in a swine model [J]. Exp Mol Med，2018，50（9）：114.