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大气超细颗粒物(PM)暴露可导致气道损伤,但相关分子机制尚未被阐明。浙医二院-浙江大学呼吸病研究所沈华浩教授课题组,通过在人支气管上皮细胞(human bronchial epithelial cells)和小鼠模型上的研究,首次证实细胞自噬在PM诱导的气道炎症和气道粘液高分泌中起到关键作用,而抑制细胞自噬作用或许能起到一定的治疗效果,该研究成果近期已发表于国际权威的生物细胞学专业期刊——《自噬》。这也是科学家们在全球范围内首次证实细胞自噬行为与雾霾导致的气道疾病之间的关系。

Environmental ultrafine particulate matter (PM) is capable of inducing airway injury, while the detailed molecular mechanisms remain largely unclear. Here, Shen. et al demonstrate pivotal roles of autophagy in regulation of inflammation and mucus hyperproduction induced by PM containing environmentally persistent free radicals in human bronchial epithelial (HBE) cells and in mouse airways. These data indicate that autophagy is required for PM-induced airway epithelial injury, and that inhibition of autophagy exerts therapeutic benefits for PM-induced airway inflammation and mucus hyperproduction, although they are differentially orchestrated by the autophagic flux. ? ?

At present, this achievement has been published in the international authoritative professional journal of cell biology-- Autophagy. This is the first time to confirm the relationship between autophagy and airway diseases caused by PM.?

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