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作 者:毛炜婷 张若琪 赵玥雯 黄珊 MAO Weiting;ZHANG Ruoqi;ZHAO Yuewen;HUANG Shan(Hospital of Stomatology,the First Affiliated Hospital of Jinan University,Clinical Research Platform for Interdiscipline of Stomatology,Jinan University,School of Stomatology,Jinan University,Guangzhou 510632,China)
机构地区:[1]暨南大学附属第一医院口腔医院,暨南大学口腔交叉学科临床研究平台,暨南大学口腔医学院,广东广州510632
出 处:《中国病理生理杂志》2025年第2期388-393,共6页Chinese Journal of Pathophysiology
基 金:国家自然科学基金青年科学基金项目(No.82104938)。
摘 要:牙周炎是一种由微生物群落失调和宿主免疫反应改变引发的慢性炎症性疾病,以牙槽骨吸收为主要特征,是牙齿松动和脱落的主要原因之一。组织蛋白酶K(cathepsin K,CTSK)是由破骨细胞高度表达的一种胶原酶,可以直接降解胶原蛋白,间接增强破骨细胞活性。CTSK的表达水平随牙周炎症的发展而改变。牙周炎病变组织中Toll样受体(Toll-like receptors,TLRs)表达上调,病原体相关分子模式的生物大分子与对应的TLRs受体结合并启动下游免疫途径,促进核因子κB受体活化因子配体(receptor activator of nuclear factor-κB ligand,RANKL)依赖性破骨细胞增多及CTSK的大量表达。通过调控CTSK可以实现对牙槽骨吸收过程的干预。本文总结CTSK在牙周炎致病机制中的作用以及以CTSK为治疗靶点的研究进展,以期为牙周炎的治疗提供参考。Periodontitis is a chronic inflammatory disease primarily triggered by dysregulation of microbial communities and altered host immune response.It is clinically presented by alveolar bone resorption,which is one of the main causes of loosening of teeth and tooth loss.Cathepsin K(CTSK)is a highly expressed collagenase produced by osteoclasts and can directly degrade matrix collagen proteins and indirectly increase osteoclast activity.The expression level of CTSK fluctuates in response to the progression of periodontal inflammation.The expression of Toll-like receptors is upregulated in periodontitis lesions.Pathogen-associated molecular pattern binds to relevant TLRs,initiating downstream immune pathways that promote receptor activator of nuclear factor-κB ligand-dependent osteoclastogenesis,along with increased expression of CTSK.Intervening in the process of alveolar bone resorption can be achieved through the regulation of CTSK.This paper provides a summary of the pathogenic mechanism of CTSK in periodontitis and highlights the research progress regarding the use of CTSK as a therapeutic target.The aim is to offer insights and references for the treatment of periodontitis.
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