2018
DOI: 10.18632/aging.101532
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Abstract: Aging is the main risk factor for the development of idiopathic pulmonary fibrosis (IPF), a progressive and usually lethal lung disorder. Although the pathogenic mechanisms are uncertain, endoplasmic reticulum (ER) stress and impaired proteostasis that have been linked with aging are strongly associated with the pathogenesis of IPF. Using the Atg4b-deficient mice as a model, that partially reproduces the autophagy deficient conditions reported in aging and IPF lungs, we show for the first time how autophagy im… Show more

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Cited by 14 publications
(11 citation statements)
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References 42 publications
(74 reference statements)
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“…Subsequent experiments were focused on mechanism/s that are involved in Parkin degradation, including potential impact of endoplasmic reticulum (ER) stress, a relevant mechanism of AECs dysfunction in lung injury and fibrosis 15 , 42 , 43 . We found that Tunicamycin-mediated ER stress effectively triggered degradation of Parkin in AECs (Fig.…”
Section: Resultsmentioning
confidence: 99%
“…Subsequent experiments were focused on mechanism/s that are involved in Parkin degradation, including potential impact of endoplasmic reticulum (ER) stress, a relevant mechanism of AECs dysfunction in lung injury and fibrosis 15 , 42 , 43 . We found that Tunicamycin-mediated ER stress effectively triggered degradation of Parkin in AECs (Fig.…”
Section: Resultsmentioning
confidence: 99%
“…ATG4B is a cysteine protease that belongs to the LC3 conjugation system and mediates the cycle of LC3-lipidation and delipidation, thereby representing a central node in the regulation of the autophagic flux. 12,13 Control lungs exhibited a low level of ATG4B staining in macrophages, whereas other cell types were negative (Fig. 3A).…”
Section: Resultsmentioning
confidence: 95%
“…ATG4B has also an esterase activity that hydrolyzes the phospholipid link in LC3B-II, recycling LC3B to its cytoplasmic free form. 12,13 We also chose the autophagy receptor p62 that directly interacts with LC3B and functions as a key cargo adaptor for the degradation of several substrates. 6 8…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…In contrast, ATG4B‐deficient mice display more extensive and severe fibrosis with bleomycin or tunicamycin treatment and increased inflammatory response induced by lipopolysaccharides. These findings explain the role of autophagy in the regulation of inflammatory and fibrotic responses 150,151,194 . Chen et al observed that Egr‐1 upregulates ATG4B, thus inhibiting autophagy in the early stages of chronic obstructive pulmonary disease (COPD) 148 .…”
Section: Atg4 and Diseasesmentioning
confidence: 86%