ArticleJournal of vascular research2014
Increased calcification in osteoprotegerin-deficient smooth muscle cells: Dependence on receptor activator of NF-κB ligand and interleukin 6.
Article in Journal of vascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- Pooled it
- Myocardial Perfusion in Rheumatoid Arthritis Patients: Associations with Traditional Risk Factors and Novel Biomarkers.BioMed research international · 2017Trial
- Circulating osteoprotegerin and progression of coronary artery calcification in patients with chronic kidney disease: the KoreaN Cohort Study for Outcome in Patients With Chronic Kidney Disease (KNOW-CKD).Kidney research and clinical practice · 2026Article
- The biology of lipoprotein(a): From genetics to molecular mechanisms.European journal of clinical investigation · 2026Review
- Uremic serum exposure leads to differential phenotypic switch in porcine arterial and venous smooth muscle cells.American journal of physiology. Renal physiology · 2025Article
- Association of prognostic nutritional index and severe abdominal aortic calcification in middle-aged adults: a cross-sectional study.BMC cardiovascular disorders · 2025Article
- Circulating osteoprotegerin levels and cardiovascular outcomes in patients with pre-dialysis chronic kidney disease: results from the KNOW-CKD study.Scientific reports · 2024Article
- Article
- Association between dietary vitamin C and abdominal aortic calcification among the US adults.Nutrition journal · 2023Article
- Serum OPG and RANKL Levels as Risk Factors for the Development of Cardiovascular Calcifications in End-Stage Renal Disease Patients in Hemodialysis.Life (Basel, Switzerland) · 2023Article
- Article
- von Willebrand Factor: A Central Regulator of Arteriovenous Fistula Maturation Through Smooth Muscle Cell Proliferation and Outward Remodeling.Journal of the American Heart Association · 2022Article
- Phosphate Is a Cardiovascular Toxin.Advances in experimental medicine and biology · 2022Review
- The two facets of receptor tyrosine kinase in cardiovascular calcification-can tyrosine kinase inhibitors benefit cardiovascular system?Frontiers in cardiovascular medicine · 2022Review
- Lipoprotein(a), a Lethal Player in Calcific Aortic Valve Disease.Frontiers in cell and developmental biology · 2022Review
- Restoration of 5-methoxytryptophan protects against atherosclerotic chondrogenesis and calcification in ApoEJournal of biomedical science · 2021Article
- Resveratrol Ameliorates Aortic Calcification in Ovariectomized Rats via SIRT1 Signaling.Current issues in molecular biology · 2021Article
- Bone Metabolism and RANKL/OPG Ratio in Rheumatoid Arthritis Women Treated with TNF-α Inhibitors.Journal of clinical medicine · 2021Article
- Calciprotein Particles: Balancing Mineral Homeostasis and Vascular Pathology.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Long-Term Treatment of Azathioprine in Rats Induces Vessel Mineralization.Biomedicines · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveVascular calcification is highly correlated with cardiovascular disease morbidity and mortality. Osteoprotegerin (OPG) is a secreted decoy receptor for receptor activator of NF-κB ligand (RANKL). Inactivation of OPG in apolipoprotein E-deficient (ApoE-/-) mice increases lesion size and calcification. The mechanism(s) by which OPG is atheroprotective and anticalcific have not been entirely determined. We investigated whether OPG-deficient vascular smooth muscle cells (VSMCs) are more susceptible to mineralization and whether RANKL mediates this process.
resultsLesion-free aortas from 12-week-old ApoE-/-OPG-/- mice had spotty calcification, an appearance of osteochondrogenic factors and a decrease of smooth muscle markers when compared to ApoE-/-OPG+/+ aortas. In osteogenic conditions, VSMCs isolated from ApoE-/-OPG-/- (KO-VSMC) mice deposited more calcium than VSMCs isolated from ApoE-/-OPG+/+ (WT-VSMC) mice. Gene expression and biochemical analysis indicated accelerated osteochondrogenic differentiation. Ablation of RANKL signaling in KO-VSMCs rescued the accelerated calcification. While WT-VSMCs did not respond to RANKL treatment, KO-VSMCs responded with enhanced calcification and the upregulation of osteochondrogenic genes. RANKL strongly induced interleukin 6 (IL-6), which partially mediated RANKL-dependent calcification and gene expression in KO-VSMCs.
conclusionsOPG inhibits vascular calcification by regulating the procalcific effects of RANKL on VSMCs and is thus a possible target for therapeutic intervention.
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Registered trials
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