ArticleScience advances2026
PARP1 stabilizes FOXN3 to suppress pulmonary fibrosis through p38-related feedback regulation.
Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pentasystem embolism associated with transient antiphospholipid antibodies in severe M.Frontiers in immunology · 2026Pooled it
- Mechanistic insights into the renoprotective effects of rutin-loaded selenium nanoparticles against 5-fluorouracil toxicity via regulation of Nrf2/Keap1, NF-κB/NLRP3, and PERK pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Modulation of p38 MAPK signaling in spinal cord injury by curcumin: targeting inflammation, oxidative stress, and apoptosis.Inflammopharmacology · 2026Review
- Can the Prognostic Nutritional Index Be a Predictor of Acute Exacerbation of Idiopathic Pulmonary Fibrosis?Biomedicines · 2026Article
- Association Between DLCO and Echocardiographic Right Ventricular-Pulmonary Arterial Coupling in Idiopathic Pulmonary Fibrosis.Journal of clinical medicine · 2026Article
- The Gut-Lung Microbiome Axis in Alveolar Stem Cell Regeneration and Lung Repair.Microorganisms · 2026Review
- Recent advances in biomarkers for cardiac fibrosis.Frontiers in cardiovascular medicine · 2026Review
- Carbapenem-resistant hypervirulentFrontiers in microbiology · 2026Review
Corrections and comments
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Authors and funding
16 authors.
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No grant is acknowledged in the PubMed record.
Abstract
The transcriptional repressor forkhead box N3 (FOXN3) has been reported to suppress pulmonary fibrosis by inhibiting Smad transcriptional activity. However, FOXN3 becomes unstable in response to profibrotic stimuli. This study identifies poly(ADP-ribose) polymerase-1 (PARP1) as a stabilizing partner of FOXN3, preventing its degradation by blocking p38-mediated phosphorylation. Lung-specific knockout (KO) of PARP1 promotes the development of pulmonary fibrosis by reducing the abundance of FOXN3. Conditional overexpression of FOXN3 notably mitigates pulmonary fibrosis resulting from PARP1 KO by impeding Smad signaling, underscoring the critical role of the PARP1-FOXN3 axis in pulmonary fibrosis. Mechanistically, p38 is a Smad response gene that is transcriptionally repressed by the PARP1/FOXN3 complex. The disruption of PARP1 or FOXN3 increases p38 expression, which in turn facilitates FOXN3 degradation through a feedback mechanism. This cascade activates Smad signaling, leading to a profibrotic response and myofibroblast activation. Notably, levels of PARP1 and FOXN3 are significantly reduced in patients with pulmonary fibrosis, highlighting PARP1's crucial role in suppressing the disease by regulating FOXN3-mediated Smad signaling.
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