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获得性胆脂瘤上皮细胞过度增殖:细胞增殖信号通路的作用

Acquired cholesteatoma epithelial hyperproliferation: Roles of cell proliferation signal pathways.

作者信息

Xie Shumin, Xiang Yuyan, Wang Xiaoli, Ren Hongmiao, Yin Tuanfang, Ren Jihao, Liu Wei

机构信息

Department of Otolaryngology-Head and Neck Surgery, Xiangya Hospital of Central South University, Changsha, Hunan Province, China.

Department of Human Anatomy, University of South China, Hengyang, Hunan Province, China.

出版信息

Laryngoscope. 2016 Aug;126(8):1923-30. doi: 10.1002/lary.25834. Epub 2016 Mar 15.

Abstract

OBJECTIVES/HYPOTHESIS: To review the recent cell proliferation signal pathways in the etiopathogenesis of acquired middle ear cholesteatoma.

DATA SOURCES

PubMed (to September 2015).

REVIEW METHODS

Articles about cell proliferation signal pathways in the etiopathogenesis of acquired cholesteatoma and treatment advances were searched in the PubMed database, from which 73 were included in this review.

RESULTS

The exact underlying cellular and molecular mechanism of acquired cholesteatoma still remains unknown. Recent research tends to regard the proliferation of cholesteatoma epithelial cells as the mechanism of cholesteatoma pathogenesis. Cell proliferation signal pathways including epidermal growth factor receptor/phosphoinositide 3-kinase/protein kinase B signal pathway, mitogen-activated protein kinase signal pathway, interleukin-6/signal transducer and activator of transcription 3 signal pathway, inhibitor of DNA binding/differentiation-1/nuclear factor-κB/cyclinD1 signal pathway, microRNA-mediated proliferation signal pathway, and keratinocyte growth factor/keratinocyte growth factor receptor signal pathway have been proven to play important roles in acquired middle ear cholesteatoma.

CONCLUSIONS

This review outlines the main biological properties of certain cell proliferation signal pathways, aiming to facilitate the development of potential therapeutic targets for intratympanic drug therapy for the nonsurgical or complementary treatment of cholesteatoma.

LEVEL OF EVIDENCE

NA Laryngoscope, 126:1923-1930, 2016.

摘要

目的/假设:综述获得性中耳胆脂瘤发病机制中近期的细胞增殖信号通路。

数据来源

PubMed(截至2015年9月)。

综述方法

在PubMed数据库中检索有关获得性胆脂瘤发病机制中细胞增殖信号通路及治疗进展的文章,本综述纳入其中73篇。

结果

获得性胆脂瘤确切的细胞和分子机制仍不清楚。近期研究倾向于将胆脂瘤上皮细胞的增殖视为胆脂瘤发病机制。包括表皮生长因子受体/磷脂酰肌醇3激酶/蛋白激酶B信号通路、丝裂原活化蛋白激酶信号通路、白细胞介素-6/信号转导及转录激活因子3信号通路、DNA结合抑制因子/分化因子-1/核因子-κB/细胞周期蛋白D1信号通路、微小RNA介导的增殖信号通路以及角质形成细胞生长因子/角质形成细胞生长因子受体信号通路在内的细胞增殖信号通路已被证实在获得性中耳胆脂瘤中起重要作用。

结论

本综述概述了某些细胞增殖信号通路的主要生物学特性,旨在促进为胆脂瘤非手术或辅助治疗的鼓室内药物治疗开发潜在治疗靶点。

证据水平

NA 喉科学,126:1923 - 1930,2016年。

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