Carvalhana G, Auquit-Auckbur I, Milliez P-Y
Service de chirurgie plastique et de la main, CHU de Rouen, 4, rue de Germont, 76000 Rouen, France.
Chir Main. 2011 Sep;30(4):239-45. doi: 10.1016/j.main.2011.03.002. Epub 2011 Apr 28.
From Baron Dupuytren's historical description up to the advent of molecular biology, many hypotheses about the etiology of Dupuytren's disease have been proposed. This bibliography of the last ten years' publications describes tissue anomalies from the macroscopic down to the ultrastructural level of pathology. The myofibroblast, which is the principal cell of the disease, is the seat of genetics anomalies involving proto-oncogenes (c-myc and MafB). Similarly, glycoproteins implicated in cellular adhesion like fibronectins and catenins are modified and overexpressed in the disease. Extracellular proteins of the metalloproteinase family exhibit many dysfunctions responsible for collagenic proliferation. Finally, growth factors like Transforming Growth Factor (TGF) and Epidermal Growth Factor (EGF) receptor maintain and worsen the disease and could be therapeutic targets in the future.
从迪皮特朗男爵的历史描述到分子生物学的出现，人们提出了许多关于迪皮特朗病病因的假说。这份过去十年出版物的参考文献描述了从宏观到病理学超微结构水平的组织异常。肌成纤维细胞是该病的主要细胞，是涉及原癌基因（c-myc和MafB）的基因异常所在。同样，参与细胞黏附的糖蛋白如纤连蛋白和连环蛋白在该病中发生修饰并过度表达。金属蛋白酶家族的细胞外蛋白表现出许多导致胶原增殖的功能障碍。最后，转化生长因子（TGF）和表皮生长因子（EGF）受体等生长因子维持并加重该病，可能成为未来的治疗靶点。
