BAG3: An enticing therapeutic target for idiopathic pulmonary fibrosis

被引:0
作者
Chillappagari, Shashipavan [1 ,2 ,3 ]
Guenther, Andreas [1 ,2 ,3 ,4 ,5 ,6 ,7 ]
Mahavadi, Poornima [1 ,2 ,3 ,8 ]
机构
[1] Justus Liebig Univ JLU Giessen, Dept Internal Med, Giessen, Germany
[2] Univ Giessen & Marburg Lung Ctr UGMLC, Giessen, Germany
[3] German Ctr Lung Res DZL, Giessen, Germany
[4] European IPF Network, Giessen, Germany
[5] European IPF Registry, Giessen, Germany
[6] JLU, Cardiopulm Inst CPI, Giessen, Germany
[7] Agaples Evangel Krankenhaus Mittelhessen, Lung Clin, Giessen, Germany
[8] Gaffkystr 11, D-35392 Giessen, Germany
关键词
autophagy; BAG3; idiopathic pulmonary fibrosis; therapeutic intervention; AUTOPHAGY; MACROAUTOPHAGY; EXPRESSION; PROMOTES;
D O I
10.1002/jcb.30446
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Idiopathic pulmonary fibrosis (IPF) is a dreadful and fatal disease of unknown etiology, for which no cure exists. Autophagy, a lysosomal cellular surveillance pathway is insufficiently activated in both alveolar epithelial type II cells and fibroblasts of IPF patient lungs. Fine-tuning this pathway may result in the degradation of the accumulated cargo and influence cell fate. Based on our previous data, we here present our view on modulating autophagy via a unique co-chaperone, namely Bcl2-associated athanogene3 (BAG3) in IPF and discuss about how repurposing drugs that modulate this pathway may emerge as a promising novel therapeutic approach for IPF.
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页数:6
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