ArticleThe Journal of clinical investigation2019
Cleavage factor 25 deregulation contributes to pulmonary fibrosis through alternative polyadenylation.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 75 citations in OpenAlex.
- Nanopore full-length sequencing reveals Nudt21 knockdown drives genome-wide 3'UTR shortening and transcriptome reprogramming in mouse hepatocytes.BMC genomics · 2026Article
- CFIm25-dependent alternative polyadenylation in AKT2 mRNA programs macrophage polarization.iScience · 2026Article
- Article
- Modulation of Nudt21 levels reveals dose-dependent roles of alternative polyadenylation in tissue regeneration.Nature communications · 2026Article
- CPSF6-mediated alternative polyadenylation of RUNX1 to regulate silica-induced pulmonary fibrosis progression.Respiratory research · 2026Article
- Myofibroblast-Derived Extracellular Vesicles Drive Profibrotic Cascade Amplification in Pulmonary Fibrosis via the Nestin-Rab7 Axis.Journal of extracellular vesicles · 2026Article
- Alternative Polyadenylation Signatures Distinguish Maladaptive Right Ventricular Remodeling in Pulmonary Hypertension: Implications for RNA-Based Diagnostics and Therapeutics.British journal of biomedical science · 2026Article
- Alternative cleavage and polyadenylation: key regulatory mechanisms in health and disease.RNA biology · 2025Review
- NUDT21 Regulates Macrophage Cytokine Responses via Alternative Polyadenylation in ARDS.Research square · 2025Article
- Loss of CFIm activates YAP/TAZ and connects mRNA cleavage and polyadenylation inhibition to BRCAness.bioRxiv : the preprint server for biology · 2025Article
- Alternative Polyadenylation Contributes to Fibroblast Senescence in Pulmonary Fibrosis.Aging cell · 2025Article
- From Epithelium to Therapy: Transitional Cells in Lung Fibrosis.American journal of respiratory cell and molecular biology · 2025Review
- Review
- The alternative polyadenylation regulator CFIm25 promotes macrophage differentiation and activates the NF-κB pathway.Cell communication and signaling : CCS · 2025Article
- Characterization and molecular targeting of CFIm25 (NUDT21/CPSF5) mRNA using miRNAs.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- TRIM65 deficiency alleviates renal fibrosis through NUDT21-mediated alternative polyadenylation.Cell death and differentiation · 2024Article
- Unraveling the role of MiR-181 in skin fibrosis pathogenesis by targeting NUDT21.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Integration of apaQTL and eQTL analysis reveals novel SNPs associated with occupational pulmonary fibrosis risk.Archives of toxicology · 2024Article
- Dexmedetomidine alleviates pulmonary fibrosis through the ADORA2B-Mediated MAPK signaling pathway.Respiratory research · 2023Article
- NUDT21 alters glioma migration through differential alternative polyadenylation of LAMC1.Journal of neuro-oncology · 2023Article
Corrections and comments
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Authors and funding
25 authors at 6 institutions in 2 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic and deadly disease with a poor prognosis and few treatment options. Pathological remodeling of the extracellular matrix (ECM) by myofibroblasts is a key factor that drives disease pathogenesis, although the underlying mechanisms remain unknown. Alternative polyadenylation (APA) has recently been shown to play a major role in cellular responses to stress by driving the expression of fibrotic factors and ECMs through altering microRNA sensitivity, but a connection to IPF has not been established. Here, we demonstrate that CFIm25, a global regulator of APA, is down-regulated in the lungs of patients with IPF and mice with pulmonary fibrosis, with its expression selectively reduced in alpha-smooth muscle actin (α-SMA) positive fibroblasts. Following the knockdown of CFIm25 in normal human lung fibroblasts, we identified 808 genes with shortened 3'UTRs, including those involved in the transforming growth factor-β signaling pathway, the Wnt signaling pathway, and cancer pathways. The expression of key pro-fibrotic factors can be suppressed by CFIm25 overexpression in IPF fibroblasts. Finally, we demonstrate that deletion of CFIm25 in fibroblasts or myofibroblast precursors using either the Col1a1 or the Foxd1 promoter enhances pulmonary fibrosis after bleomycin exposure in mice. Taken together, our results identified CFIm25 down-regulation as a novel mechanism to elevate pro-fibrotic gene expression in pulmonary fibrosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.