ArticleMolecular medicine (Cambridge, Mass.)2024
PRMT3 methylates HIF-1α to enhance the vascular calcification induced by chronic kidney disease.
Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 17 citations in OpenAlex.
- Vascular calcification: pathogenic mechanisms, signaling crosstalk and translational therapeutics.Signal transduction and targeted therapy · 2026Review
- PRMT3-Mediated Arginine Methylation Stabilizes PCSK9 to Promote Aortic Valve Calcification.Circulation · 2026Article
- Protein arginine methyltransferases in cancer: mechanisms, functions, and therapeutic opportunities.Journal of biomedical science · 2026Review
- Histone arginine demethylase JMJD7 promotes bone formation through regulating α-Ketoglutarate metabolism.Cell death and differentiation · 2026Article
- PRMT3 in cancer: arginine methylation as a driver of tumor metabolism, immune evasion, and therapeutic resistance.Frontiers in immunology · 2026Review
- Leptin Regulates Intervertebral Disc Calcification and Ossification by Promoting Glycolysis Through OCN/HIF-1α Axis.Journal of cellular and molecular medicine · 2026Article
- Interfacial Coordination-Engineered Emulgel Modulates the Osteo-Immune Microenvironment in Periodontitis Treatment Via HIF1 Signaling Pathway-Induced Metabolic Reprogramming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Phosphate salt selection affects mortality and vascular calcification in the adenine-induced chronic kidney disease mouse model.American journal of physiology. Heart and circulatory physiology · 2025Article
- Therapeutic targeting of protein arginine methyltransferases reduces breast cancer progression by disrupting angiogenic pathways.Biochemistry and biophysics reports · 2025Review
- Protein arginine methyltransferases as regulators of cellular stress.Experimental neurology · 2025Review
- PRMT3 and CARM1: Emerging Epigenetic Targets in Cancer.Journal of cellular and molecular medicine · 2025Review
- Shengqing Jiangzhuo Capsule Alleviates Intestinal Inflammation in Chronic Kidney Disease by Downregulating CHAC1 to Inactivate the HIF-1 Pathway.Mediators of inflammation · 2025Article
- PRMT3 at the crossroads of inflammation: dual roles in metabolic reprogramming and immune dysregulation in chronic diseases.Frontiers in immunology · 2025Review
- Enzymatic post-translational modifications of proteins in chronic kidney disease: mechanisms, regulation, and clinical significance.Frontiers in pharmacology · 2025Review
- The Physiological Functions and Therapeutic Potential of Hypoxia-Inducible Factor-1α in Vascular Calcification.Biomolecules · 2024Review
- Metabolites and metabolism in vascular calcification: links between adenosine signaling and the methionine cycle.American journal of physiology. Heart and circulatory physiology · 2024Review
- Dickkopf-1 (DKK1) blockade mitigates osteogenesis imperfecta (OI) related bone disease.Molecular medicine (Cambridge, Mass.) · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMedial vascular calcification is commonly identified in chronic kidney disease (CKD) patients and seriously affects the health and life quality of patients. This study aimed to investigate the effects of protein arginine methyltransferase 3 (PRMT3) on vascular calcification induced by CKD.
methodsA mice model of CKD was established with a two-step diet containing high levels of calcium and phosphorus. Vascular smooth muscle cells (VSMCs) were subjected to β-glycerophosphate (β-GP) treatment to induce the osteogenic differentiation as an in vitro CKD model.
resultsPRMT3 was upregulated in VSMCs of medial artery of CKD mice and β-GP-induced VSMCs. The inhibitor of PRMT3 (SGC707) alleviated the vascular calcification and inhibited the glycolysis of CKD mice. Knockdown of PRMT3 alleviated the β-GP-induced osteogenic transfomation of VSMCs by the repression of glycolysis. Next, PRMT3 interacted with hypoxia-induced factor 1α (HIF-1α), and the knockdown of PRMT3 downregulated the protein expression of HIF-1α by weakening its methylation. Gain of HIF-1α reversed the PRMT3 depletion-induced suppression of osteogenic differentiation and glycolysis of VSMCs.
conclusionThe inhibitory role of PRMT3 depletion was at least mediated by the regulation of glycolysis upon repressing the methylation of HIF-1α.
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