ArticleCardiovascular research2024
Smooth muscle cell-specific matrix metalloproteinase 3 deletion reduces osteogenic transformation and medial artery calcification.
Article in Cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 20 citations in OpenAlex.
- CNN3 promotes vascular smooth muscle cells proliferation and migration to deteriorate atherosclerosis by β-catenin signaling pathway.Atherosclerosis plus · 2026Article
- Serum Mucin-1 (CA15-3) in Relation to Pulse Pressure Amplification in Untreated Chinese Patients.Journal of clinical hypertension (Greenwich, Conn.) · 2026Article
- Research Progress on the Molecular Mechanism of LRP1 and TGFβ-PDGFRβ Signaling Network in Atherosclerosis and Vascular Remodeling.International journal of molecular sciences · 2026Review
- Lanthanum Chloride in Vascular Calcification: Effects on Nano-Hydroxyapatite and PPARγ/Wnt/β-Catenin.FASEB bioAdvances · 2026Article
- YAK577 Attenuates Vascular Calcification by Targeting an MMP14-NOX2/ROS Axis in VSMCs and a Vitamin DAntioxidants (Basel, Switzerland) · 2026Article
- Deciphering the molecular landscape of aortic aging: a meta-analysis of bulk RNA sequencing studies in mice.GeroScience · 2026Article
- Calcific Aortopathy in Response to Aging and Injury.Circulation · 2026Review
- Decoding vascular calcification: mechanistic insights and translational strategies.Cellular and molecular life sciences : CMLS · 2026Review
- Endothelial BMP6 Drives Hemodynamic-Dependent VSMCs Calcification in Carotid Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Exosomal hsa-miR-299-3p from endothelium mediates high phosphorus-induced vascular calcification in mice model of CKD via phosphorylated JAK2/STAT5 pathway.Frontiers in pharmacology · 2026Article
- Mechanisms of vascular calcification: cellular phenotype switching drives matrix remodeling and mineralized microenvironment formation.Frontiers in cardiovascular medicine · 2026Review
- Treadmill exercise ameliorates atherogenesis and vascular inflammation in ApoEScientific reports · 2025Article
- Irisin targets the HK1-glycolysis-NLRP3 pyroptosis axis to prevent chronic kidney disease-associated vascular calcification.Renal failure · 2025Article
- Vascular Smooth Muscle Cell Metabolic Reprogramming in Arteriovenous Fistula Failure.Biomedicines · 2025Review
- Matrix metalloproteinase-3 promotes arteriovenous fistula failure by regulating FAK-AKT signaling.bioRxiv : the preprint server for biology · 2025Article
- The Non-Traditional Cardiovascular Culprits in Chronic Kidney Disease: Mineral Imbalance and Uremic Toxin Accumulation.International journal of molecular sciences · 2025Review
- Review
- Understanding the Prevalence of Medial Arterial Calcification Among Complex Reconstructive Patients: Insights from a Decade of Experience at a Tertiary Limb Salvage Center.Journal of clinical medicine · 2025Article
- Calcification of the elastic component: the impact on the cardiovascular system.Frontiers in cardiovascular medicine · 2025Review
- GSDME in cardiovascular diseases: research system and contemporary progress.Frontiers in immunology · 2025Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
aimsVascular calcification is highly prevalent in atherosclerosis, diabetes, and chronic kidney disease. It is associated with increased morbidity and mortality in patients with cardiovascular disease. Matrix metalloproteinase 3 (MMP-3), also known as stromelysin-1, is part of the large matrix metalloproteinase family. It can degrade extracellular matrix components of the arterial wall including elastin, which plays a central role in medial calcification. In this study, we sought to determine the role of MMP-3 in medial calcification. METHODS AND
resultsWe found that MMP-3 was increased in rodent models of medial calcification as well as in vascular smooth muscle cells (SMCs) cultured in a phosphate calcification medium. It was also highly expressed in calcified tibial arteries in patients with peripheral arterial disease (PAD). Knockdown and inhibition of MMP-3 suppressed phosphate-induced SMC osteogenic transformation and calcification, whereas the addition of a recombinant MMP-3 protein facilitated SMC calcification. In an ex vivo organ culture model and a rodent model of medial calcification induced by vitamin D3, we found that MMP-3 deficiency significantly suppressed medial calcification in the aorta. We further found that medial calcification and osteogenic transformation were significantly reduced in SMC-specific MMP-3-deficient mice, suggesting that MMP-3 in SMCs is an important factor in this process.
conclusionThese findings suggest that MMP-3 expression in vascular SMCs is an important regulator of medial calcification and that targeting MMP-3 could provide a therapeutic strategy to reduce it and address its consequences in patients with PAD.
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