Chillappagari, ShashipavanShashipavanChillappagariGuenther, AndreasAndreasGuentherMahavadi, PoornimaPoornimaMahavadi2023-12-052023-12-052023https://jlupub.ub.uni-giessen.de/handle/jlupub/18744http://dx.doi.org/10.22029/jlupub-18108Idiopathic 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.enNamensnennung - Nicht kommerziell - Keine Bearbeitungen 4.0 InternationalautophagyBAG3idiopathic pulmonary fibrosistherapeutic interventionddc:610