ArticleCommunications biology2025
PLAC8 attenuates pulmonary fibrosis and inhibits apoptosis of alveolar epithelial cells via facilitating autophagy.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- VCP at the crossroads of UPS and autophagy in cancer.Genes & diseases · 2027Review
- Targeting the senescence‒autophagy axis via p16Signal transduction and targeted therapy · 2026Article
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- LncRNA HOXA11-AS promotes idiopathic pulmonary fibrosis progression via sponging miR-148a-3p and regulating SMAD2.Hereditas · 2026Article
- Integrative multi-omics analysis reveals microbiota alterations and clinical indicators predictive of pulmonary fibrosis progression following SARS-CoV-2 infection.Briefings in bioinformatics · 2026Article
- How cells die determines the consequences of tissue repair: roles of programmed cell death in lung injury on the progression of pulmonary fibrosis.Molecular and cellular biochemistry · 2026Review
- Emodin: A Promising Natural Compound for Combating Fibrotic Diseases.Current medical science · 2026Review
- Effects of faba beans (Food chemistry. Molecular sciences · 2025Article
- Homocysteine Exacerbates Pulmonary Fibrosis via Orchestrating Syntaxin 17 Homocysteinylation of Alveolar Type II Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Autophagy in the lung: guardian of homeostasis or driver of disease.Autophagy reports · 2025Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is an irreversible lung condition that progresses over time, which ultimately results in respiratory failure and mortality. In this study, we found that PLAC8 was downregulated in the lungs of IPF patients based on GEO data, in bleomycin (BLM)-induced lungs of mice, and in primary murine alveolar epithelial type II (pmATII) cells and human lung epithelial cell A549 cells. Overexpression of PLAC8 facilitated autophagy and inhibited apoptosis of pmATII cells and A549 cells in vitro. Moreover, inhibition of autophagy or overexpression of p53 partially abolished the effects of PLAC8 on cell apoptosis. ATII cell-specific overexpression of PLAC8 alleviated BLM-induced pulmonary fibrosis in mice. Mechanistically, PLAC8 interacts with VCP-UFD1-NPLOC4 complex to promote p53 degradation and facilitate autophagy, resulting in inhibiting apoptosis of alveolar epithelial cells and attenuating pulmonary fibrosis. In summary, these findings indicate that PLAC8 may be a key target for therapeutic interventions in pulmonary fibrosis.
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