ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
PRMT1 Ablation in Endothelial Cells Causes Endothelial Dysfunction and Aggravates COPD Attributable to Dysregulated NF-κB Signaling.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Exhaled breath volatile organic compounds (VOCs) detection methods: GC-MS versus eNose in COPD diagnosis-a systematic review and meta-analysis.BMC pulmonary medicine · 2025Pooled it
- Connexin 43 Loss in Endothelial Progenitors Facilitates Functional Airway Adaptation After Lung Injury.Research square · 2026Article
- Association between the endothelial activation and stress index and 28-day all-cause mortality in critically ill patients with chronic obstructive pulmonary disease: a retrospective cohort study and predictive model establishment based on machine learning.BMC pulmonary medicine · 2026Article
- New approaches to uncover COPD pathobiology and develop therapies.JCI insight · 2026Review
- Expression and Significance of Protein Arginine Methyltransferase 1 in the Serum of Patients with Diabetes Kidney Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- PDHA1 Hyperactivation Orchestrates Metabolic Reprogramming Promoting Endothelial Senescence.Research (Washington, D.C.) · 2026Article
- Development and validation of a nomogram based on immune-inflammation-nutrition indictors for predicting 28-day mortality in sepsis patients with severe fungal pneumonia.Frontiers in cellular and infection microbiology · 2026Article
- E-Selectin-Targeted Nanomicelles via Sialic Acid Conjugation for Anti-Inflammatory Efficacy and Alleviating the Progression of Metabolic-Associated Steatotic Liver Disease.Biomaterials research · 2026Article
- Analysis of risk factors for calf muscular vein thrombosis in elderly patients with acute exacerbation of chronic obstructive pulmonary disease.Frontiers in cardiovascular medicine · 2026Article
- Review
- The Role of Protein Arginine Methylation as a Post-Translational Modification in Cellular Homeostasis and Disease.Biology · 2025Review
- The Mechanism and Potential Therapeutic Strategies of Vascular Aging.Aging medicine (Milton (N.S.W)) · 2025Review
- Immunoinflammation and post-translational modifications in the aging process.Journal of translational medicine · 2025Review
- PRMT1 Ablation in Endothelial Cells Causes Endothelial Dysfunction and Aggravates COPD Attributable to Dysregulated NF-κB Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The promoting role of protein arginine methyltransferase 1 in cervical cancer: Mechanisms of angiogenesis and immune evasion.CytoJournal · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Endothelial dysfunction and senescence are pivotal in pulmonary diseases, including chronic obstructive pulmonary disease (COPD). Protein arginine methyltransferase 1 (PRMT1) is the major enzyme responsible for asymmetric arginine dimethylation and plays a role in diverse biological processes, including cardiovascular function. Yet, its role in endothelial cells (ECs) remains poorly understood. Here, the role of PRMT1 is investigated in ECs, particularly in the context of COPD pathogenesis. Endothelial-specific PRMT1 knockout mice exhibit pulmonary hemorrhage, inflammation, barrier disruption, and apoptosis, accompanied by hyperactivation of nuclear factor kappa B (NF-κB). Bulk RNA sequencing of whole lungs and single-cell RNA sequencing of pulmonary ECs reveal that endothelial PRMT1 ablation results in a major alteration in inflammation-related gene expression. In a COPD model, PRMT1 deficiency aggravates the COPD phenotypes, including enlarged alveolar spaces, increased cell death, and senescence. PRMT1 inhibition in ECs exacerbates tumor necrosis factor alpha-triggered EC senescence and dysfunction attributable to NF-κB hyperactivation. PRMT1 as a critical regulator of pulmonary EC function, preventing NF-κB-driven endothelial dysfunction and senescence is highlighted here.
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Registered trials
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