ArticleJournal of vascular research2012
RANKL enhances macrophage paracrine pro-calcific activity in high phosphate-treated smooth muscle cells: dependence on IL-6 and TNF-α.
Article in Journal of vascular research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 99 citations in OpenAlex.
- Review
- Rapidly Progressive Medial Calcific Sclerosis in a Dialysis Patient.Diagnostics (Basel, Switzerland) · 2026Article
- Adipose-Derived Proinflammatory Visfatin Promotes Vascular Calcification via TLR4 and is Suppressed by Empagliflozin.Inflammation · 2026Article
- Peripheral Vascular Calcification.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Review
- Bone and Cardiometabolic Connection: Crosstalk between Osteoporosis and Atherosclerosis.Cell biochemistry and biophysics · 2025Review
- Multiple Ectopic calcifications in end-stage renal disease: role of inflammation and partial reversibility with intensified peritoneal dialysis-a case report.BMC nephrology · 2025Article
- Regulation of Vascular Calcification by M1-Type Macrophage-Derived Semaphorin 4D.International journal of molecular sciences · 2025Article
- Association of skin-advanced glycation end products, IMT complex, and bone mineral density in patients with type 1 diabetes.Frontiers in endocrinology · 2025Article
- Macrophages as key modulators of calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025Review
- Bisphenol F exposure induced vascular toxicity through intestinal microbiota imbalance.Frontiers in microbiology · 2025Article
- Macrophage NLRP3-dependent IL-1β production contributes to aortic fibrosis in heart failure with preserved ejection fraction.Acta biochimica et biophysica Sinica · 2024Article
- The Physiological Functions and Therapeutic Potential of Hypoxia-Inducible Factor-1α in Vascular Calcification.Biomolecules · 2024Review
- LPS-induced senescence of macrophages aggravates calcification and senescence of vascular smooth muscle cells via IFITM3.Renal failure · 2024Article
- Vascular calcification: from the perspective of crosstalk.Molecular biomedicine · 2023Review
- CXCR6 Mediates Pressure Overload-Induced Aortic Stiffness by Increasing Macrophage Recruitment and Reducing Exosome-miRNA29b.Journal of cardiovascular translational research · 2023Article
- Drug screening in zebrafish larvae reveals inflammation-related modulators of secondary damage after spinal cord injury in mice.Theranostics · 2023Article
- Macrophage death in atherosclerosis: potential role in calcification.Frontiers in immunology · 2023Review
- Two-faced Janus: the dual role of macrophages in atherosclerotic calcification.Cardiovascular research · 2022Review
- The Role of Interleukin-6 Family Members in Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundVascular calcification is highly correlated with cardiovascular disease (CVD) morbidity and mortality, and it is associated with inflammation. Receptor activator of NF-ĸB ligand (RANKL) inhibition in vivo has been shown to reduce vascular calcification in a mouse model of atherosclerosis. Therefore, we tested the hypothesis that RANKL regulates smooth muscle cell (SMC) calcification by modulating macrophage production of pro-calcific cytokines.
methodsWe used a bone marrow-derived macrophage (BMDM)/SMC co-culture system and examined the effects of RANKL on BMDM activation and SMC matrix calcification.
resultsTreatment with RANKL alone did not stimulate SMC calcification induced by elevated phosphate. BMDMs differentiated with macrophage colony-stimulating factor and placed in co-culture with SMCs increased phosphate-induced SMC calcification. RANKL added to the BMDM/SMC co-cultures further enhanced SMC calcification. Treatment of BMDMs with RANKL resulted in increased expression of IL-6 and TNF-α. Thus, increased expression of these pro-calcific cytokines in macrophages may mediate RANKL-induced SMC calcification in a paracrine fashion. Addition of neutralizing IL-6 and TNF-α antibodies together with RANKL treatment significantly reduced the RANKL induction of SMC calcification.
conclusionRANKL activation of pro-inflammatory and pro-calcific pathways in macrophages may contribute to vascular calcification and inflammation.
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Registered trials
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.