瘢痕疙瘩发病机制的研究进展
摘要
<正>瘢痕疙瘩是瘢痕的一种,属病理性瘢痕,其特点是过度生长,超出创伤的范围,侵犯临近组织,不能自行消退,手术切除后易复发。瘢痕疙瘩不仅影响外观,而且可能影响患者的功能,时间久远的瘢痕疙瘩合并感染以后甚至发生恶变,形成瘢痕癌,给患者身心带来极大的危害。对于本病的发病机制,国内外有不同的观点和看法,尚没有定论。回顾近年文献,国内外学者对瘢痕疙瘩的发病机制进行了更深入的研究,也取得一些进展,现综述如下。
引文
[1]Koonin AJ.The aeiology of keloids:a review of the literature and a new hypothesis[J].South Afr Med J,1964,38:913-916.
[2]Brissett AE,Sherris DA.Scar contractures,hypertrophic scars,and keloids[J].Facial Plast Surg,2001,17:263-272.
[3]Ak9z T,Gideroglu K,Akan M.Combination of different techniques for the treatment of earlobe keloids[J].Aesthetic Plast Surg,2002,26:184-188.
[4]Kelly AP.Medical and surgical therapies for keloids.Dermatol Ther[J].2004,17:212-218.
[5]Ramakrishnan KM,Thomas KP,Sundararajan CR.Study of 1,000patients with keloids in South India[J].Plast Reconstr Surg,1974,53:276-280.
[6]Zhu F,Wu B,Li P,et al.Assoiation study comfirmed susceptibility Loci with keloid in the Chinese Han population[J].PLoS One,2013,8(5):e62377.
[7]刘永波,高建华,刘晓军,等.瘢痕疙瘩临床表型与p53基因72位编码子基因多态性的相关性分析[J].中国修复重建外科杂志,2008,22(12):1433-1436.
[8]吴严,刘佳丽,陈晶,等.外周血p53基因多态性与中国人瘢痕疙瘩相关性的Meta分析[J].中国循证医学杂志,201l,l1(6):651-654.
[9]Lu L,Sanlis AS,Liu WR,et al.The temporal effects at anti-TGFbeta 1,2,and 3monoclonal antibody on wound healing and hypertrophic scar formation[J].JAm Coil Surg,2005,201(3):391-397.
[10]刘波,果磊.SiRNA-Smad3沉默人瘢痕疙瘩成纤维细胞中Smad3对纤维连接蛋白及I型胶原表达的影响[J].重庆医科大学学报,2010,35(4):522-526.
[11]鲁峰,高建华.携带Fas基因重组腺病毒治疗瘢痕疙瘩的体内实验研究[J].中华外科杂志,2007,45(15):1058-1060.
[12]于冬梅,郝立君,肖志波,等.Survivin和Caspase-3在病理性瘢痕成纤维细胞中的表达及其意义[J].中国美容整形外科杂志,2008,19(1):77-79.
[13]Lim CP,Phan TT,Lim IJ,et al.Stat3contributes to keloid pathogenesis via promoting collagen production,cell proliferation and migration[J].Oncogene,2006,25(39):5416-5425.
[14]王齐,聂芳菲,赵霞,等.periostin在过度增生性瘢痕的表达及其与TGF-131和受体的相关性[J].中华整形外科杂志,2007,23(3):229-232.
[15]黄勇,邢新.端粒酶、bcl-2和p53在瘢痕疙瘩组织中的表达及意义[J].中华实验外科杂志,2006,23(5):635.
[16]洪学哲,李小静,宁金龙,等.TSG.6在病理性瘢痕中的表达及意义[J].安徽医科大学学报,2013,48(6):486-487.
[17]Marmeros AG,Norris JE,Olsen BR,et al.Chnical genetics of familial Keliods[J].Arch Dermatol,2001,137(11):1429.
[18]Mameros AG,Noms JE,Watanabe S,et al.Geflome scaHs provide evidence for keloid susceptibility loci on chromosomes 2q23and7ql1[J].Invest Dermatol,2004,122(5):1126-1132.
[19]陈阳,高建华,刘晓军.中国汉族瘢痕疙瘩家系的遗传学特征研究[J].南方医科大学学报,2007,7(27):976-979.
[20]Smith CJ,Smith JC,Finn MC.The possible role ofmast cells(allergy)in the production of keloid and hypertrophic scar[J].J Bum CareRehabil,1987,8(2):126-131.
[21]Harty M,Neff AW,King Mw,et al.Regeneration or scarring:an immunologic perspective[J].Dev Dyn,2003,226(2):268-279.
[22]Shaker SA,Ayuob NN,Hajrah NH,et al.Cell Talk:A PhenomenonObserved in the Keloid Scar by Immunohistochemical Study[J].Appllmmuno histochem-MolMorphol,2011,19(2):153-159.
[23]杨登山,肖敏勤.细胞因子在瘢痕治疗中作用的研究进展[J].中国伤残医学,2014,22(3):277-278.
[24]赵自然,刘鹤松,张舵,等.人参皂苷Rg3对免耳增生性瘢痕的抑制作用[J].吉林大学学报,2008,34(4):628-630.
[25]Kieran I,Knock A,Bush J,et al.1nterleukin-10redu~es searformation in both animal and human cutaneous wounds:Results of two preclinical and phase II randomized control studies[J].Wound Repair Regen,2013,2l(3):428-436.
[26]吴泽勇,张培华,李瑾,等.IL-18在病理性瘢痕中的表达及其生物学意义[J].中国美容医学,2014,23(6):454-457.
[27]卫裴,梁杰.IL-24抗肿瘤机制及其对瘢痕疙瘩作用研究进展[J].齐齐哈尔医学院学报,2013,34(1):83-85.
[28]Sidgwick GP,Bayat A.Extracellular matrix moleculesimplicated in hypertrophic and keloid scarring[J].JEADV,2012,26(2):141-l52.
[29]刘琦,胡志英,郭鹏年.瘢痕疙瘩的发病机制及治疗进展[J].包头医学院学报,2011,27(5):135-138.
[30]Gauglitz GG,Korting HC,Pavicic T,et al.Hypertrophic scarring and keloids:Pathomechanisms and current and emerging treatment strategies[J].Mol reed,2011,17(1-2):113-125.
[31]杨奕敏,陆树良.MMPs和创面愈合[J].中华国际医学杂志,2002,2(3):253-256.
[32]柯朝阳,曾凡倩,熊雪莲,等.单核细胞趋化蛋白-1和骨形成蛋白-7在耳部瘢痕疙瘩中的表达及意义[J].中华耳科学杂志,2012,10(4):493-497.
[33]张鹏,沈雷,李云峰,等.Tenascin C在瘢痕疙瘩成纤维细胞中表达增高及其意义[J].中国美容医学,2012,21(8):1330-1331
[34]Chen J,Zeng B,Yao H,et al.The effect of TLR4/7on the TGF—B-induced Smad signal transduction pathway in human keloid[J].Burns,2013,39(3):465-472.
[35]Lim CP,Phan 1Tr,Lim IJ,et al.Stat3contributes to keloidpathogenesis via promoting collagen production,cell proliferation and migration[J].Oncogene,2006,25(39):5416-5425.
[36]Inui S,Shono F,Nakajima.et al.Identification and characterization of cartilage oligomeric matrix protein as a novel pathogenic factorin keloids[J].Am J Pathol,2011,179(4):1951-1960.
[37]潘春梅,陈晓栋,沈聪聪,等.膜联蛋白A2在瘢痕疙瘩中的表达[J].中国皮肤性病学杂志,2013,21(11):1088-1116.
[38]徐静静,蔡景龙.瘢痕疙瘩的细胞信号转导通路的研究进展[J].Journal of Tissue Engineering and Reconstructive Surgery,2014,10(5):282-284
[39]刘畅,陈敏亮.瘢痕疙瘩发病的分子机制研究进展[J].中国美容医学,2013,22(14):1557-1560.
[40]王炜.整形外科学[M].杭州:浙江科学技术出版社,2007:437.
[41]Brody GS,Peng ST,Landel RF.The etiology ofhypertrophic scar contracture:An other view[J].Plast Reconstr Surg,1981,67:673.
[42]Huang C,Ogawa R.Fibroproliferative disorders and their mechanobio1ogy[J].Connect Tissue Res,2012,53(3):187-196.
[43]Huang C,Ogawa R.Roles of lipid metabolism in keloid development[J].Lipid Health disea,2013,12:60.
[44]刘嘉锋,张一鸣,易传勋,等,性激素受体在瘢痕中的表达及与细胞周期调控蛋白相互关系的研究[J].中华整形外科杂志,2004,20(4):265-267.
[2]Brissett AE,Sherris DA.Scar contractures,hypertrophic scars,and keloids[J].Facial Plast Surg,2001,17:263-272.
[3]Ak9z T,Gideroglu K,Akan M.Combination of different techniques for the treatment of earlobe keloids[J].Aesthetic Plast Surg,2002,26:184-188.
[4]Kelly AP.Medical and surgical therapies for keloids.Dermatol Ther[J].2004,17:212-218.
[5]Ramakrishnan KM,Thomas KP,Sundararajan CR.Study of 1,000patients with keloids in South India[J].Plast Reconstr Surg,1974,53:276-280.
[6]Zhu F,Wu B,Li P,et al.Assoiation study comfirmed susceptibility Loci with keloid in the Chinese Han population[J].PLoS One,2013,8(5):e62377.
[7]刘永波,高建华,刘晓军,等.瘢痕疙瘩临床表型与p53基因72位编码子基因多态性的相关性分析[J].中国修复重建外科杂志,2008,22(12):1433-1436.
[8]吴严,刘佳丽,陈晶,等.外周血p53基因多态性与中国人瘢痕疙瘩相关性的Meta分析[J].中国循证医学杂志,201l,l1(6):651-654.
[9]Lu L,Sanlis AS,Liu WR,et al.The temporal effects at anti-TGFbeta 1,2,and 3monoclonal antibody on wound healing and hypertrophic scar formation[J].JAm Coil Surg,2005,201(3):391-397.
[10]刘波,果磊.SiRNA-Smad3沉默人瘢痕疙瘩成纤维细胞中Smad3对纤维连接蛋白及I型胶原表达的影响[J].重庆医科大学学报,2010,35(4):522-526.
[11]鲁峰,高建华.携带Fas基因重组腺病毒治疗瘢痕疙瘩的体内实验研究[J].中华外科杂志,2007,45(15):1058-1060.
[12]于冬梅,郝立君,肖志波,等.Survivin和Caspase-3在病理性瘢痕成纤维细胞中的表达及其意义[J].中国美容整形外科杂志,2008,19(1):77-79.
[13]Lim CP,Phan TT,Lim IJ,et al.Stat3contributes to keloid pathogenesis via promoting collagen production,cell proliferation and migration[J].Oncogene,2006,25(39):5416-5425.
[14]王齐,聂芳菲,赵霞,等.periostin在过度增生性瘢痕的表达及其与TGF-131和受体的相关性[J].中华整形外科杂志,2007,23(3):229-232.
[15]黄勇,邢新.端粒酶、bcl-2和p53在瘢痕疙瘩组织中的表达及意义[J].中华实验外科杂志,2006,23(5):635.
[16]洪学哲,李小静,宁金龙,等.TSG.6在病理性瘢痕中的表达及意义[J].安徽医科大学学报,2013,48(6):486-487.
[17]Marmeros AG,Norris JE,Olsen BR,et al.Chnical genetics of familial Keliods[J].Arch Dermatol,2001,137(11):1429.
[18]Mameros AG,Noms JE,Watanabe S,et al.Geflome scaHs provide evidence for keloid susceptibility loci on chromosomes 2q23and7ql1[J].Invest Dermatol,2004,122(5):1126-1132.
[19]陈阳,高建华,刘晓军.中国汉族瘢痕疙瘩家系的遗传学特征研究[J].南方医科大学学报,2007,7(27):976-979.
[20]Smith CJ,Smith JC,Finn MC.The possible role ofmast cells(allergy)in the production of keloid and hypertrophic scar[J].J Bum CareRehabil,1987,8(2):126-131.
[21]Harty M,Neff AW,King Mw,et al.Regeneration or scarring:an immunologic perspective[J].Dev Dyn,2003,226(2):268-279.
[22]Shaker SA,Ayuob NN,Hajrah NH,et al.Cell Talk:A PhenomenonObserved in the Keloid Scar by Immunohistochemical Study[J].Appllmmuno histochem-MolMorphol,2011,19(2):153-159.
[23]杨登山,肖敏勤.细胞因子在瘢痕治疗中作用的研究进展[J].中国伤残医学,2014,22(3):277-278.
[24]赵自然,刘鹤松,张舵,等.人参皂苷Rg3对免耳增生性瘢痕的抑制作用[J].吉林大学学报,2008,34(4):628-630.
[25]Kieran I,Knock A,Bush J,et al.1nterleukin-10redu~es searformation in both animal and human cutaneous wounds:Results of two preclinical and phase II randomized control studies[J].Wound Repair Regen,2013,2l(3):428-436.
[26]吴泽勇,张培华,李瑾,等.IL-18在病理性瘢痕中的表达及其生物学意义[J].中国美容医学,2014,23(6):454-457.
[27]卫裴,梁杰.IL-24抗肿瘤机制及其对瘢痕疙瘩作用研究进展[J].齐齐哈尔医学院学报,2013,34(1):83-85.
[28]Sidgwick GP,Bayat A.Extracellular matrix moleculesimplicated in hypertrophic and keloid scarring[J].JEADV,2012,26(2):141-l52.
[29]刘琦,胡志英,郭鹏年.瘢痕疙瘩的发病机制及治疗进展[J].包头医学院学报,2011,27(5):135-138.
[30]Gauglitz GG,Korting HC,Pavicic T,et al.Hypertrophic scarring and keloids:Pathomechanisms and current and emerging treatment strategies[J].Mol reed,2011,17(1-2):113-125.
[31]杨奕敏,陆树良.MMPs和创面愈合[J].中华国际医学杂志,2002,2(3):253-256.
[32]柯朝阳,曾凡倩,熊雪莲,等.单核细胞趋化蛋白-1和骨形成蛋白-7在耳部瘢痕疙瘩中的表达及意义[J].中华耳科学杂志,2012,10(4):493-497.
[33]张鹏,沈雷,李云峰,等.Tenascin C在瘢痕疙瘩成纤维细胞中表达增高及其意义[J].中国美容医学,2012,21(8):1330-1331
[34]Chen J,Zeng B,Yao H,et al.The effect of TLR4/7on the TGF—B-induced Smad signal transduction pathway in human keloid[J].Burns,2013,39(3):465-472.
[35]Lim CP,Phan 1Tr,Lim IJ,et al.Stat3contributes to keloidpathogenesis via promoting collagen production,cell proliferation and migration[J].Oncogene,2006,25(39):5416-5425.
[36]Inui S,Shono F,Nakajima.et al.Identification and characterization of cartilage oligomeric matrix protein as a novel pathogenic factorin keloids[J].Am J Pathol,2011,179(4):1951-1960.
[37]潘春梅,陈晓栋,沈聪聪,等.膜联蛋白A2在瘢痕疙瘩中的表达[J].中国皮肤性病学杂志,2013,21(11):1088-1116.
[38]徐静静,蔡景龙.瘢痕疙瘩的细胞信号转导通路的研究进展[J].Journal of Tissue Engineering and Reconstructive Surgery,2014,10(5):282-284
[39]刘畅,陈敏亮.瘢痕疙瘩发病的分子机制研究进展[J].中国美容医学,2013,22(14):1557-1560.
[40]王炜.整形外科学[M].杭州:浙江科学技术出版社,2007:437.
[41]Brody GS,Peng ST,Landel RF.The etiology ofhypertrophic scar contracture:An other view[J].Plast Reconstr Surg,1981,67:673.
[42]Huang C,Ogawa R.Fibroproliferative disorders and their mechanobio1ogy[J].Connect Tissue Res,2012,53(3):187-196.
[43]Huang C,Ogawa R.Roles of lipid metabolism in keloid development[J].Lipid Health disea,2013,12:60.
[44]刘嘉锋,张一鸣,易传勋,等,性激素受体在瘢痕中的表达及与细胞周期调控蛋白相互关系的研究[J].中华整形外科杂志,2004,20(4):265-267.