ArticleScientific reports2022
Loss of PRMT2 in myeloid cells in normoglycemic mice phenocopies impaired regression of atherosclerosis in diabetic mice.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- S-Adenosylmethionine-Dependent Methylation, Protein Arginine Methyltransferases and Cardiovascular Diseases.Biomolecules · 2026Review
- Protein arginine methyltransferases as metabolic regulators: many roles beyond cancer.Science China. Life sciences · 2026Review
- PRMT2 Aggravates Pressure Overload-induced Cardiac Remodeling by Promoting Endothelial Phenotypic Transition via Snail1 Methylation.Cardiovascular drugs and therapy · 2026Article
- The Role of Protein Arginine Methylation as a Post-Translational Modification in Cellular Homeostasis and Disease.Biology · 2025Review
- Immunometabolic reprogramming in diabetic osteomyelitis: from mechanisms to therapeutics.Frontiers in cellular and infection microbiology · 2025Review
- Arginine Methylation of β-Catenin Induced by PRMT2 Aggravates LPS-Induced Cognitive Dysfunction and Depression-Like Behaviors by Promoting Ferroptosis.Molecular neurobiology · 2024Article
- Protein arginine methyltransferase 2 controls inflammatory signaling in acute myeloid leukemia.Communications biology · 2024Article
- PRMT2 silencing regulates macrophage polarization through activation of STAT1 or inhibition of STAT6.BMC immunology · 2024Article
- An Updated Review on the Significance of DNA and Protein Methyltransferases and De-methylases in Human Diseases: From Molecular Mechanism to Novel Therapeutic Approaches.Current medicinal chemistry · 2024Review
- A case of malonyl coenzyme A decarboxylase deficiency with novel mutations and literature review.Frontiers in pediatrics · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The regression, or resolution, of inflammation in atherosclerotic plaques is impaired in diabetes. However, the factors mediating this effect remain incomplete. We identified protein arginine methyltransferase 2 (PRMT2) as a protein whose expression in macrophages is reduced in hyperglycemia and diabetes. PRMT2 catalyzes arginine methylation to target proteins to modulate gene expression. Because PRMT2 expression is reduced in cells in hyperglycemia, we wanted to determine whether PRMT2 plays a causal role in the impairment of atherosclerosis regression in diabetes. We, therefore, examined the consequence of deleting PRMT2 in myeloid cells during the regression of atherosclerosis in normal and diabetic mice. Remarkably, we found significant impairment of atherosclerosis regression under normoglycemic conditions in mice lacking PRMT2 (Prmt2
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