ArticleCell death & disease2022
PRMT5 critically mediates TMAO-induced inflammatory response in vascular smooth muscle cells.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- Review
- S-Adenosylmethionine-Dependent Methylation, Protein Arginine Methyltransferases and Cardiovascular Diseases.Biomolecules · 2026Review
- Decoding the Gut-Fat-Heart Axis: From Molecular Communication Networks to Clinical Translation Strategies.International journal of molecular sciences · 2026Review
- The N‑Glycoproteomic Landscape of the Lung in Monocrotaline-Induced Pulmonary Arterial Hypertension.ACS omega · 2026Article
- The essential role of hydrogen gas recycling by gut microbes in reducing deuterium load in host mitochondria: is trimethylamine oxide a deuterium sensor?Metabolomics : Official journal of the Metabolomic Society · 2026Review
- Gut microbiota-derived metabolites as immune modulators in aging and age-related chronic inflammatory diseases.Ageing research reviews · 2026Review
- Chromatin Remodeling in VSMC Phenotype Switching During Vascular Remodeling: From Mechanism to Therapeutic Potential.Biomolecules · 2026Review
- Gut Microbiota-Derived Trimethylamine N-Oxide and NT-proBNP in Heart Failure: A Critical Review of Diagnostic and Prognostic Value.Biomedicines · 2026Review
- Protein arginine methyltransferases in cardiovascular disease: mechanisms, therapeutic potential, and future directions.Frontiers in physiology · 2026Review
- Establishment of a mouse model of TMAO-induced cardiac injury and application of MICT intervention.Animal models and experimental medicine · 2026Article
- Discovery and Mechanism of 16-19F, a Novel Synthetic Lethal Inhibitor of the PRMT5•MTA Complex in MTAP-Deleted Cancer Cells.ACS chemical biology · 2025Article
- Gut microbiota-derived trimethylamine-N-oxide inhibits SIRT1 to regulate SM22α-mediated smooth muscle cell inflammation and promote atherosclerosis progression.Journal of cell communication and signaling · 2025Article
- Low-Molecular-Weight Compounds Produced by the Intestinal Microbiota and Cardiovascular Disease.International journal of molecular sciences · 2024Review
- Role of Gut Microbial Metabolites in Cardiovascular Diseases-Current Insights and the Road Ahead.International journal of molecular sciences · 2024Review
- Protein Arginine Methyltransferases: Emerging Targets in Cardiovascular and Metabolic Disease.Diabetes & metabolism journal · 2024Review
- Trends in gut-heart axis and heart failure research (1993-2023): A bibliometric and visual analysis.Heliyon · 2024Article
- Gut-immune axis and cardiovascular risk in chronic kidney disease.Clinical kidney journal · 2024Review
- Epigenetic regulation of vascular smooth muscle cell phenotypic switch and neointimal formation by PRMT5.Cardiovascular research · 2023Article
- Is the Gut Microbiome Implicated in the Excess Risk of Hypertension Associated with Obstructive Sleep Apnea? A Contemporary Review.Antioxidants (Basel, Switzerland) · 2023Review
- Gut-Derived Metabolite, Trimethylamine-N-oxide (TMAO) in Cardio-Metabolic Diseases: Detection, Mechanism, and Potential Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A high plasma level of the choline-derived metabolite trimethylamine N-oxide (TMAO) is closely related to the development of cardiovascular disease. However, the underlying mechanism remains unclear. In the present study, we demonstrated that a positive correlation of protein arginine methyltransferase 5 (PRMT5) expression and TMAO-induced vascular inflammation, with upregulated vascular cell adhesion molecule-1 (VCAM-1) expression in primary rat and human vascular smooth muscle cells (VSMC) in vitro. Knockdown of PRMT5 suppressed VCAM-1 expression and the adhesion of primary bone marrow-derived macrophages to TMAO-stimulated VSMC. VSMC-specific PRMT5 knockout inhibited vascular inflammation with decreased expression of VCAM-1 in mice. We further identified that PRMT5 promoted VCAM-1 expression via symmetrical demethylation of Nuclear factor-κB p65 on arginine 30 (R30). Finally, we found that TMAO markedly induced the expression of nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4) and production of reactive oxygen species, which contributed to PRMT5 expression and subsequent VCAM-1 expression. Collectively, our data provide novel evidence to establish a Nox4-PRMT5-VCAM-1 in mediating TMAO-induced VSMC inflammation. PRMT5 may be a potential target for the treatment of TMAO-induced vascular diseases.
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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.