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摘要: 尿道手术后尿道瘢痕的形成是常见的并发症，常常影响尿道患者的术后康复，一直是泌尿外科医生面临的十分棘手的问题。由于其病因的复杂性，导致治疗效果往往不佳。本文通过对尿道瘢痕相关文献的分析，了解影响尿道瘢痕形成的一些因素，从而为尿道瘢痕的临床预防和治疗奠定理论依据。Abstract: The formation of urethral scar is a common complication after urethral surgery. It often affects the recovery of patients who had experienced urethral surgery and remains a major challenge for urologists. It often leads a dissatisfied treatment effect since the formation of urethral scar have a complicated etiology. This paper want to introduce some of factors which play an important role in the formation of urethral scar by reviewing the related literature about urethral scar, and provide a theory evidence to prevent and treat urethral stricture scar.
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Key words:
- urethral scar /
- fibroblast /
- collagen /
- transforming growth factor-β
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[1] Brown J J, Ollier W E, Thomson W, et al. Positive association of HLA-DRB1*15 with keloid disease in Caucasians[J]. Int J Immunogenet, 2008, 35:303-307.
[2] 王国胜, 李正天, 姜涛, 等. 家族遗传与非家族遗传性病理性瘢痕的基因芯片谱研究[J]. 哈尔滨医科大学学报, 2010, 44(2):142-147.
[3] Salcido R S. The cicatrix:the critical functional stage of wound healing[J]. Adv Skin Wound Care, 2008, 21:402, 404.
[4] Louw L. Keloids in rural black South Africans. Part 1:general overview and essential fatty acid hypotheses for keloid formation and prevention[J]. Prostaglandins Leukot Essent Fatty Acids, 2000, 63:237-245.
[5] Marneros A G, Norris J E, Watanabe S, et al. Genome scans provide evidence for keloid susceptibility loci on chromosomes 2q23 and 7p11[J]. J Invest Dermatol, 2004, 122:1126-1132.
[6] 刘晓军, 高建华, 宋玫, 等. 中国汉族瘢痕疙瘩家系易感基因位点的定位分析研究[J]. 中国美容整形外科杂志, 2008, 19(3):179-183.
[7] 程飚, 付小兵, 盛志勇, 等. 瘢痕组织中α-平滑肌肌动蛋白的表达与细胞凋亡的关系[J]. 中国病理生理杂志, 2002, 18(11):1333-1336.
[8] Luo S, Benathan M, Raffoul W, et al. Abnormal balance between proliferation and apoptotic cell death in fibroblasts derived from keloid lesions[J]. Plast Reconstr Surg, 2001, 107:87-96.
[9] Funayama E, Chodon T, Oyama A, et al. Keratinocytes promote proliferation and inhibit apoptosis of the underlying fibroblasts:an important role in the pathogenesis of keloid[J]. J Invest Dermatol, 2003, 121:1326-1331.
[10] Chen W, Fu X B, Ge S L, et al. Development of gene microarray in screening differently expressed genes in keloid and normal-control skin[J]. Chin Med J (Engl), 2004, 117:877-881.
[11] Song J, Xu H, Lu Q, et al. Madecassoside suppresses migration of fibroblasts from keloids:involvement of p38 kinase and PI3K signaling pathways[J]. Burns, 2012, 38:677-684.
[12] 袁敬东, 胡葵葵, 胡琼华, 等. 瘢痕疙瘩胶原代谢机制研究进展[J]. 实用临床医学, 2003, 4(3):129-131.
[13] 黄翔, 张红英, 扬宇如, 等. 尿道瘢痕组织的病理学研究[J]. 临床泌尿外科杂志, 2003, 18(10):610-612.
[14] Boyd J I 3rd, Wongworawat M D. High-pressure pulsatile lavage causes soft tissue damage[J]. Clin Orthop Relat Res, 2004, (427):13-17.
[15] Verrecchia F, Mauviel A, Farge D. Transforming growth factor-beta signaling through the Smad proteins:role in systemic sclerosis[J]. Autoimmun Rev, 2006, 5:563-569.
[16] Schiller M, Javelaud D, Mauviel A. TGF-beta-induced SMAD signaling and gene regulation:consequences for extracellular matrix remodeling and wound healing[J]. J Dermatol Sci, 2004, 35:83-92.
[17] Sadick H, Herberger A, Riedel K, et al. TGF-beta1 antisense therapy modulates expression of matrix metalloproteinases in keloid-derived fibroblasts[J]. Int J Mol Med, 2008, 22:55-60.
[18] Ihn H. Pathogenesis of fibrosis:role of TGF-beta and CTGF[J]. Curr Opin Rheumatol, 2002, 14:681-685.
[19] Klass B R, Grobbelaar A O, Rolfe K J. Transforming growth factor beta1 signalling, wound healing and repair:a multifunctional cytokine with clinical implications for wound repair, a delicate balance[J]. Postgrad Med J, 2009, 85:9-14.
[20] del Re E, Babitt JL, Pirani A, et al. In the absence of type III receptor, the transforming growth factor (TGF)-beta type II-B receptor requires the type I receptor to bind TGF-beta2[J]. J Biol Chem, 2004, 279:22765-22772.
[21] Derynck R, Zhang Y E. Smad-dependent and Smad-independent pathways in TGF-beta family signalling[J]. Nature, 2003, 425:577-584.
[22] Yamashita M, Fatyol K, Jin C, et al. TRAF6 mediates Smad-independent activation of JNK and p38 by TGF-beta[J]. Mol Cell, 2008, 31:918-924.
[23] Yu L, Hébert M C, Zhang Y E. TGF-beta receptor-activated p38 MAP kinase mediates Smad-independent TGF-beta responses[J]. EMBO J, 2002, 21:3749-3759.
[24] Chen W, Frangogiannis N G. Fibroblasts in post-infarction inflammation and cardiac repair[J]. Biochim Biophys Acta, 2012, Sep 7.
[25] 周庆余, 刘齐贵, 郭瑞威. 尿液刺激在尿道术后瘢痕形成中的作用[J]. 昆明医学院学报, 2011, 32(4):77-80.
[26] Ten Dijke P, Goumans M J, Itoh F, et al. Regulation of cell proliferation by Smad proteins[J]. J Cell Physiol, 2002, 191:1-16.
[27] Schiller M, Javelaud D, Mauviel A. TGF-beta-induced SMAD signaling and gene regulation:consequences for extracellular matrix remodeling and wound healing[J]. J Dermatol Sci, 2004, 35:83-92.
[28] 胡小勇, 徐月敏. 尿道狭窄的流行病学、病因学、组织学和分类[M]//徐月敏. 尿道狭窄修复重建外科学. 北京:人民卫生出版社, 2010:10-13.
[29] Bourboulia D, Stetler-Stevenson W G. Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs):Positive and negative regulators in tumor cell adhesion[J]. Semin Cancer Biol, 2010, 20:161-168.
[30] Stetler-Stevenson W G. The tumor microenvironment:regulation by MMP-independent effects of tissue inhibitor of metalloproteinases-2[J]. Cancer Metastasis Rev, 2008, 27:57-66.
[31] Ulrich D, Ulrich F, Unglaub F, et al. Matrix metalloproteinases and tissue inhibitors of metalloproteinases in patients with different types of scars and keloids[J]. J Plast Reconstr Aesthet Surg, 2010, 63:1015-1021.
[32] 黄翔, 魏大鹏, 杨宇如, 等. 尿道瘢痕组织胶原酶活性及TIMP-1表达的研究[J]. 中国修复重建外科杂志, 2003, 17(6):433-435.
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