ArticleNature communications2022
The arginine methyltransferase PRMT7 promotes extravasation of monocytes resulting in tissue injury in COPD.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 2 of them syntheses that pooled it.
What it found
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Who cites it
78 citing papers in PubMed, 2 syntheses or guidelines pooled it, 115 citations in OpenAlex.
- A systematic review of protein post-translational modifications in sepsis.Molecular biology reports · 2025Pooled it
- Recent Evidences of Epigenetic Alterations in Chronic Obstructive Pulmonary Disease (COPD): A Systematic Review.International journal of molecular sciences · 2025Pooled it
- PRMT7 restricts CD8+ T cells expansion via the NF-ΚB pathway.Nature communications · 2026Article
- Histone Post-Translational Modifications Regulating Ferroptosis: The Molecular Mechanisms and Disease Associations.Cell biochemistry and function · 2026Review
- Role of PRMT5 in regulating ferritinophagy during Mycobacterium tuberculosis infection.PLoS pathogens · 2026Article
- PRMT5 Mediates Sepsis-Associated Lung Injury by Modulating JAK1 Arginine Methylation: A Mechanism Study.The Kaohsiung journal of medical sciences · 2026Article
- Review
- Adenine nucleotide translocase 2 (ANT2) deficiency reprograms ferroptosis in alveolar progenitor cells to promote emphysema.bioRxiv : the preprint server for biology · 2026Article
- Dapagliflozin binds PRMT7 to inhibit p38 MAPK phosphorylation and macrophage foam cell formation in atherosclerosis.iScience · 2026Article
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Review
- TRPML1 suppresses pulmonary fibrosis by limiting collagen and elastin deposition.The EMBO journal · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Protein Arginine Methyltransferases in γ-Globin Regulation and Sickle Cell Disease: Emerging Connections to Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Review
- New approaches to uncover COPD pathobiology and develop therapies.JCI insight · 2026Review
- Cystatin C prevents tissue injury after lung transplantation.Life science alliance · 2026Article
- Epigenetic and post-translational regulatory networks of ferroptosis in the tumor immune microenvironment.Experimental hematology & oncology · 2026Review
- Multi-omics to study chronic respiratory diseases and viral infections.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Critical Biological Functions and Clinical Implications of Epigenetic-Related Candidate Biomarkers in Chronic Obstructive Pulmonary Disease: Integrated Machine Learning Screening and Basic Experimental Validation.International journal of chronic obstructive pulmonary disease · 2026Article
- Unified platform for multiplex immunofluorescence across liver tissues and engineered models.eGastroenterology · 2026Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
50 authors at 15 institutions in 7 countries.
Funding
Abstract
Extravasation of monocytes into tissue and to the site of injury is a fundamental immunological process, which requires rapid responses via post translational modifications (PTM) of proteins. Protein arginine methyltransferase 7 (PRMT7) is an epigenetic factor that has the capacity to mono-methylate histones on arginine residues. Here we show that in chronic obstructive pulmonary disease (COPD) patients, PRMT7 expression is elevated in the lung tissue and localized to the macrophages. In mouse models of COPD, lung fibrosis and skin injury, reduced expression of PRMT7 associates with decreased recruitment of monocytes to the site of injury and hence less severe symptoms. Mechanistically, activation of NF-κB/RelA in monocytes induces PRMT7 transcription and consequential mono-methylation of histones at the regulatory elements of RAP1A, which leads to increased transcription of this gene that is responsible for adhesion and migration of monocytes. Persistent monocyte-derived macrophage accumulation leads to ALOX5 over-expression and accumulation of its metabolite LTB4, which triggers expression of ACSL4 a ferroptosis promoting gene in lung epithelial cells. Conclusively, inhibition of arginine mono-methylation might offer targeted intervention in monocyte-driven inflammatory conditions that lead to extensive tissue damage if left untreated.
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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.