参考文献/References:
[1]Polster SP, Cao Y, Carroll T, et al. Trial readiness in cavernous angiomas with symptomatic hemorrhage (CASH)[J]. Neurosurgery, 2019, 84(4): 954-964.
[2]Detter MR, Snellings DA, Marchuk DA. Cerebral cavernous malformations develop through clonal expansion of mutant endothelial cells [J]. Circ Res, 2018, 123(10): 1143-1151.
[3]Padarti A, Zhang J. Recent advances in cerebral cavernous malformation research [J]. Vessel Plus, 2018, 2: 21.
[4]Abdelilah-Seyfried S, Tournier-Lasserve E, Derry WB. Blocking signalopathic events to treat cerebral cavernous malformations [J]. Trends Mol Med, 2020, 26(9): 874-887.
[5]Li J, Zhao Y, Coleman P, et al. Low fluid shear stress conditions contribute to activation of cerebral cavernous malformation signalling pathways [J]. Biochim Biophys Acta Mol Basis Dis, 2019, 1865(11): 165519.
[6]Zhou Z, Tang AT, Wong WY, et al. Cerebral cavernous malformations arise from endothelial gain of MEKK3-KLF2/4 signalling [J]. Nature, 2016, 532(7597): 122-126.
[7]Maddaluno L, Rudini N, Cuttano R, et al. EndMT contributes to the onset and progression of cerebral cavernous malformations [J]. Nature, 2013, 498(7455): 492-496.
[8]Lopez-Ramirez MA, Fonseca G, Zeineddine HA, et al. Thrombospondin1 (TSP1) replacement prevents cerebral cavernous malformations [J]. J Exp Med, 2017, 214(11): 3331-3346.
[9]Abdelilah-Seyfried S, Tournier-Lasserve E, Derry WB. Blocking signalopathic events to treat cerebral cavernous malformations [J]. Trends Mol Med, 2020, 2020, 26(9): 874-887.
[10]Cuttano R, Rudini N, Bravi L, et al. KLF4 is a key determinant in the development and progression of cerebral cavernous malformations [J]. EMBO Mol Med, 2016, 8(1): 6-24.
[11]Tang AT, Choi JP, Kotzin JJ, et al. Endothelial TLR4 and the microbiome drive cerebral cavernous malformations [J]. Nature, 2017, 545(7654): 305-310.
[12]Castro M, Lavina B, Ando K, et al. CDC42 deletion elicits cerebral vascular malformations via increased MEKK3-dependent KLF4 expression[J]. Circ Res, 2019, 124(8): 1240-1252.
[13]Richardson BT, Dibble CF, Borikova AL, et al. Cerebral cavernous malformation is a vascular disease associated with activated RhoA signaling [J]. Biol Chem, 2013, 394(1): 35-42.
[14]Ma J, Sanchez-Duffhues G, Goumans MJ, et al. TGF-beta-induced endothelial to mesenchymal transition in disease and tissue engineering [J]. Front Cell Dev Biol, 2020, 8: 260.
[15]Zhang Y, Li C, Huang Y, et al. EOFAZ inhibits endothelial to mesenchymal transition through downregulation of KLF4 [J]. Int J Mol Med, 2020, 46(1): 300-310.
[16]Distefano PV, Glading AJ. VEGF signalling enhances lesion burden in KRIT1 deficient mice [J]. J Cell Mol Med, 2020, 24(1): 632-639.
相似文献/References:
[1]杜彦挺 综述 潘亚文 审校.Moyamoya病的诊断和治疗的研究进展[J].中国临床神经外科杂志,2015,(12):761.[doi:10.13798/j.issn.1009-153X.2015.12.021]
[2]陈 娟 张华楸 综述 雷 霆 审校.库欣病发病机制的研究进展[J].中国临床神经外科杂志,2015,(10):594.[doi:10.13798/j.issn.1009-153X.2015.10.006]
[3]王米君 综述 舒 凯 审校.脑膜瘤瘤周水肿的研究现状[J].中国临床神经外科杂志,2015,(05):315.[doi:10.13798/j.issn.1009-153X.2015.05.022]
[4]管得宁,张 扬,徐 运.帕金森病的发病机制及治疗研究进展[J].中国临床神经外科杂志,2016,(11):732.[doi:10.13798/j.issn.1009-153X.2016.11.031]
[5]陆丽娟,李玉凤,赵喜庆 综述,等.氯离子通道与胶质瘤的关系研究进展[J].中国临床神经外科杂志,2016,(12):803.[doi:10.13798/j.issn.1009-153X.2016.12.029]
[6]吴 超 于 涛 王振宇 段丽萍.脊髓损伤后神经源性肠功能障碍的发生机制[J].中国临床神经外科杂志,2017,(04):282.[doi:10.13798/j.issn.1009-153X.2017.04.030]
[7]吕艳霞 李安荣 杨朋磊 综述 胡钧涛 审校.炎症反应在颅内动脉瘤发生中作用的研究进展[J].中国临床神经外科杂志,2017,(05):363.[doi:10.13798/j.issn.1009-153X.2017.05.030]
[8]马 涛.颅脑损伤后凝血功能障碍的机制及干预措施[J].中国临床神经外科杂志,2017,(08):601.[doi:10.13798/j.issn.1009-153X.2017.08.030]
[9]田 杨 综述,史怀璋 审校.非编码RNA参与颅内动脉瘤病理机制的研究进展[J].中国临床神经外科杂志,2018,(10):701.[doi:10.13798/j.issn.1009-153X.2018.10.021]
[10]曾子桓 张 灏 陈伟强 魏梁锋 王守森.颅脑损伤后继发性脑损伤发病机制的研究进展[J].中国临床神经外科杂志,2019,(12):777.[doi:10.13798/j.issn.1009-153X.2019.12.022]