热休克蛋白47在病理性瘢痕生成中的作用机制的探讨

发布时间：2018-09-05 10:26

【摘要】：研究背景对于病理性瘢痕的研究一直是整形外科乃至整个外科界的焦点,由于其发病机制十分复杂,至今为止仍无明确的病因学诊断,也没有一种普遍有效的治疗方法。大量研究结果表明,胶原蛋白的异常合成与沉积是许多纤维化反应疾病的病理基础,同时也是病理性瘢痕形成的重要原因。热休克蛋白47(heat shock protein,HSP47)是一种分子量为47KD的热休克蛋白,属于小分子量HSP家族。HSP47存在于胶原蛋白分泌细胞的内质网(ER)内,与前胶原特异性结合,参与前胶原的折叠、装配、修饰、转运等过程,被认为是胶原特异性分子伴侣,在胶原合成及纤维化病理过程中发挥着重要作用。国外有多项研究证实,抑制HSP47的表达,可抑制胶原合成,减弱纤维化程度。如在肾小球肾炎大鼠模型以及大鼠切口愈合实验中,局部注入HSP47反义寡核苷酸,可有效减轻了肾
[Abstract]:Background the study of pathological scar has been the focus of plastic surgery and even the whole surgical field, because of its pathogenesis is very complex, So far, there is no clear etiological diagnosis and no universal and effective treatment. A large number of studies have shown that the abnormal synthesis and deposition of collagen are the pathological basis of many fibrosis reaction diseases, and are also the important causes of pathological scar formation. Heat shock protein 47 (heat shock protein,HSP47) is a heat shock protein with a molecular weight of 47KD. It belongs to the small molecular weight HSP family. HSP47 exists in the endoplasmic reticulum (ER) of collagen secretory cells. It binds specifically with procollagen and participates in the folding, assembly and modification of procollagen. Transport is considered to be a collagen-specific molecular chaperone, which plays an important role in collagen synthesis and pathological process of fibrosis. Many studies abroad have confirmed that inhibiting the expression of HSP47 can inhibit collagen synthesis and reduce the degree of fibrosis. For example, in the rat model of glomerulonephritis and in the wound healing experiment, HSP47 antisense oligodeoxynucleotides were injected locally, and the kidney was effectively alleviated.
【学位授予单位】：四川大学
【学位级别】：博士
【学位授予年份】：2005
【分类号】：R363

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