气道杯状细胞持续性诱导：治疗干预途径
2018/01/15
摘要
杯状细胞分化调节失控导致气道粘液过度生成和滞留，而这一现象也是多种慢性气道疾病的基本特征。就目前情况看，减少粘液聚集的治疗策略主要集中在改变粘液本身的特性，或控制粘液刺激性细胞因子的生成。本文就参与杯状细胞分化过程中失调节的主要信号通路进行小结，并着重强调针对这一病理状态的既往和新型的治疗策略。
Persistent induction of goblet cell differentiation in the airways: Therapeutic approaches.
Pharmacol Ther. 2017 Dec 26. pii: S0163-7258(17)30306-6. doi: 10.1016/j.pharmthera.2017.12.009. [Epub ahead of print]
Reid AT, Veerati PC, Gosens R, Bartlett NW, Wark PA, Grainge CL, Stick SM, Kicic A, Moheimani F, Hansbro PM, Knight DA.
Abstract
Dysregulated induction of goblet cell differentiation results in excessive production and retention of mucus and is a common feature of several chronic airways diseases. To date, therapeutic strategies to reduce mucus accumulation have focused primarily on altering the properties of the mucus itself, or have aimed to limit the production of mucus-stimulating cytokines. Here we review the current knowledge of key molecular pathways that are dysregulated during persistent goblet cell differentiation and highlights both pre-existing and novel therapeutic strategies to combat this pathology.
杯状细胞分化调节失控导致气道粘液过度生成和滞留，而这一现象也是多种慢性气道疾病的基本特征。就目前情况看，减少粘液聚集的治疗策略主要集中在改变粘液本身的特性，或控制粘液刺激性细胞因子的生成。本文就参与杯状细胞分化过程中失调节的主要信号通路进行小结，并着重强调针对这一病理状态的既往和新型的治疗策略。
（上海交通大学医学院附属瑞金医院呼吸与危重症医学科 周剑平 万欢英 摘译）
（Pharmacol Ther. 2017 Dec 26. pii: S0163-7258(17)30306-6. doi: 10.1016/j.pharmthera.2017.12.009. [Epub ahead of print]）
（Pharmacol Ther. 2017 Dec 26. pii: S0163-7258(17)30306-6. doi: 10.1016/j.pharmthera.2017.12.009. [Epub ahead of print]）
Persistent induction of goblet cell differentiation in the airways: Therapeutic approaches.
Pharmacol Ther. 2017 Dec 26. pii: S0163-7258(17)30306-6. doi: 10.1016/j.pharmthera.2017.12.009. [Epub ahead of print]
Reid AT, Veerati PC, Gosens R, Bartlett NW, Wark PA, Grainge CL, Stick SM, Kicic A, Moheimani F, Hansbro PM, Knight DA.
Abstract
Dysregulated induction of goblet cell differentiation results in excessive production and retention of mucus and is a common feature of several chronic airways diseases. To date, therapeutic strategies to reduce mucus accumulation have focused primarily on altering the properties of the mucus itself, or have aimed to limit the production of mucus-stimulating cytokines. Here we review the current knowledge of key molecular pathways that are dysregulated during persistent goblet cell differentiation and highlights both pre-existing and novel therapeutic strategies to combat this pathology.
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