ArticleNature communications2024
Fibroblast-specific PRMT5 deficiency suppresses cardiac fibrosis and left ventricular dysfunction in male mice.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 24 citations in OpenAlex.
- S-Adenosylmethionine-Dependent Methylation, Protein Arginine Methyltransferases and Cardiovascular Diseases.Biomolecules · 2026Review
- RNA splicing in health and disease.Molecular biomedicine · 2026Review
- PRMT2 Aggravates Pressure Overload-induced Cardiac Remodeling by Promoting Endothelial Phenotypic Transition via Snail1 Methylation.Cardiovascular drugs and therapy · 2026Article
- Downregulation of MLL1 Promotes Intestinal Epithelial Barrier Repair Through Gata4/Bmp4 Activation to Ameliorate Crohn's Disease-Like Colitis in Mice.Cell proliferation · 2026Article
- Targeting YAP: mechanistic breakthroughs and therapeutic prospects in reversing organ fibrosis.Molecular and cellular biochemistry · 2026Review
- IRF7 links HK1-dependent histone lactylation to fibroblast activation and cardiac fibrosis.EMBO molecular medicine · 2026Article
- Intercellular chemerin-cmklr1 couples epicardial mechanosensing to fibroblasts in pressure overload.Nature communications · 2026Article
- CIITA/PRMT5 promote CD4BMC medicine · 2026Article
- The impact of inflammation, neuromodulation, and gut microbiota on developing cardiac fibrosis and hypertension.Cardiovascular research · 2026Review
- VAP1 promotes cardiac fibrosis by enabling PDGFR signaling in myofibroblasts.Experimental & molecular medicine · 2026Article
- The role of histone methylation in fibrosis and its therapeutic potential.Journal of translational medicine · 2026Review
- Protein arginine methyltransferases in cardiovascular disease: mechanisms, therapeutic potential, and future directions.Frontiers in physiology · 2026Review
- Composition and Influence of Fibrogenic Niche in Myocardial Fibrosis.Reviews in cardiovascular medicine · 2026Review
- PH20-modified exosomes loaded curcumin inhibit desmoplastic breast cancer by breaking extracellular matrix barrier and normalizing cancer-associated fibroblasts.Materials today. Bio · 2025Article
- A novel feedback loop: CELF1/circ-CELF1/BRPF3/KAT7 in cardiac fibrosis.Acta pharmaceutica Sinica. B · 2025Article
- PFKM-Driven Lactate Overproduction Promotes Atrial Fibrillation via Triggering Cardiac Fibroblasts Histone Lactylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Anti-protein arginine methyltransferase 5 (PRMT5) antibodies is associated with interstitial lung disease in rheumatoid arthritis.Scientific reports · 2025Article
- Pantothenic acid ameliorates hepatic fibrosis by targeting IGFBP6 to regulate the TGF-β/SMADs pathway.Communications biology · 2025Article
- Cardiac-specific overexpression of PRMT5 exacerbates pressure overload-induced hypertrophy and heart failure.Journal of biomedical science · 2025Article
- The E3 Ligase NEDD4L Prevents Colorectal Cancer Liver Metastasis via Degradation of PRMT5 to Inhibit the AKT/mTOR Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
Abstract
Protein arginine methyltransferase 5 (PRMT5) is a well-known epigenetic regulatory enzyme. However, the role of PRMT5-mediated arginine methylation in gene transcription related to cardiac fibrosis is unknown. Here we show that fibroblast-specific deletion of PRMT5 significantly reduces pressure overload-induced cardiac fibrosis and improves cardiac dysfunction in male mice. Both the PRMT5-selective inhibitor EPZ015666 and knockdown of PRMT5 suppress α-smooth muscle actin (α-SMA) expression induced by transforming growth factor-β (TGF-β) in cultured cardiac fibroblasts. TGF-β stimulation promotes the recruitment of the PRMT5/Smad3 complex to the promoter site of α-SMA. It also increases PRMT5-mediated H3R2 symmetric dimethylation, and this increase is inhibited by Smad3 knockdown. TGF-β stimulation increases H3K4 tri-methylation mediated by the WDR5/MLL1 methyltransferase complex, which recognizes H3R2 dimethylation. Finally, treatment with EPZ015666 significantly improves pressure overload-induced cardiac fibrosis and dysfunction. These findings suggest that PRMT5 regulates TGF-β/Smad3-dependent fibrotic gene transcription, possibly through histone methylation crosstalk, and plays a critical role in cardiac fibrosis and dysfunction.
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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.