PPARγ as a Potential Target to Treat Airway Mucus Hypersecretion in Chronic Airway Inflammatory Diseases.
PPARγ as a Potential Target to Treat Airway Mucus Hypersecretion in Chronic Airway Inflammatory Diseases.
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作者：
Shen Y;Chen L;Wang T;Wen F
气道粘液高分泌(AMH)是哮喘、囊性纤维化、慢性阻塞性肺疾病等慢性呼吸道炎症性疾病的重要病理生理特征。AMH参与慢性呼吸道炎症性疾病的发病机制，并与肺功能降低、住院率和死亡率高有关。已有研究表明，AMH可作为治疗慢性呼吸道炎症性疾病的靶点。最近的证据表明，呼吸道炎症、高反应和重塑的关键调节因子是过氧化物酶体增殖物激活受体γ(PPARγ)，它是一种配体激活的转录因子，调节脂肪细胞的分化和脂肪代谢。PPARγ在肺的结构细胞、免疫细胞和炎症细胞中表达。PPARγ参与粘蛋白的产生，PPARγ激动剂在体外和体内都能抑制粘蛋白的合成。这些发现表明，PPARγ是治疗AMH的一个新靶点，对该转录因子的进一步研究可能会导致慢性呼吸道炎症性疾病的新疗法。
Airway mucus hypersecretion (AMH) is a key pathophysiological feature of chronic airway inflammatory diseases such as bronchial asthma, cystic fibrosis, and chronic obstructive pulmonary disease. AMH contributes to the pathogenesis of chronic airway inflammatory diseases, and it is associated with reduced lung function and high rates of hospitalization and mortality. It has been suggested that AMH should be a target in the treatment of chronic airway inflammatory diseases. Recent evidence suggests that a key regulator of airway inflammation, hyperresponsiveness, and remodeling is peroxisome proliferator-activated receptor gamma (PPARγ), a ligand-activated transcription factor that regulates adipocyte differentiation and lipid metabolism. PPARγ is expressed in structural, immune, and inflammatory cells in the lung. PPARγ is involved in mucin production, and PPARγ agonists can inhibit mucin synthesis both in vitro and in vivo. These findings suggest that PPARγ is a novel target in the treatment of AMH and that further work on this transcription factor may lead to new therapies for chronic airway inflammatory diseases.
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DOI：
10.1056/nejmra0910061
发表时间：
2010-12-02
期刊：
The New England journal of medicine
影响因子：
--
作者：
Fahy JV;Dickey BF
通讯作者：
Dickey BF
DOI：
10.1165/rcmb.2005-0259oc
发表时间：
2006-08-01
影响因子：
6.4
作者：
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通讯作者：
Swinney, David C.
DOI：
10.1164/rccm.200603-381oc
发表时间：
2007-01-01
影响因子：
24.7
作者：
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通讯作者：
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影响因子：
5.6
作者：
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通讯作者：
Wen, Fu-Qiang
影响因子：
4.8
作者：
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通讯作者：
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