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自噬与肺纤维化。

Autophagy and Pulmonary Fibrosis.

机构信息

Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.

Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.

出版信息

Adv Exp Med Biol. 2020;1207:569-579. doi: 10.1007/978-981-15-4272-5_40.

Abstract

Pulmonary fibrosis is a progressive chronic inflammatory disease with a poor clinical outcome. Although pirfenidone and nintedanib have been approved by FDA to treat idiopathic pulmonary fibrosis (IPF), these drugs can only slow the progression of IPF. Autophagy plays an important role in the pathogenesis of pulmonary fibrosis. Whether the autophagic flux is blocked or not is directly related to the development direction of pulmonary fibrosis. Defining how autophagy activity regulates the pathogenesis of pulmonary fibrosis will greatly advance the progression of pulmonary fibrosis therapy.

摘要

肺纤维化是一种进行性慢性炎症性疾病,临床预后不良。尽管吡非尼酮和尼达尼布已被 FDA 批准用于治疗特发性肺纤维化(IPF),但这些药物只能减缓 IPF 的进展。自噬在肺纤维化的发病机制中起重要作用。自噬流是否受阻直接关系到肺纤维化的发展方向。明确自噬活性如何调节肺纤维化的发病机制将极大地推动肺纤维化治疗的进展。

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