ArticleAmerican journal of translational research2016
M1 macrophages promote aortic valve calcification mediated by microRNA-214/TWIST1 pathway in valvular interstitial cells.
Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 53 citations in OpenAlex.
- The Heart's Small Molecules: The Importance of MicroRNAs in Cardiovascular Health.Journal of clinical medicine · 2025Review
- Anti-IL-17 Inhibits PINK1/Parkin Autophagy and M1 Macrophage Polarization in Rheumatic Heart Disease.Inflammation · 2025Article
- Mechanical forces in the tumor microenvironment: roles, pathways, and therapeutic approaches.Journal of translational medicine · 2025Review
- The role of macrophages in vascular calcification: strategies for diagnosis and treatment.Frontiers in immunology · 2025Review
- Macrophages in Calcific Aortic Valve Disease: Paracrine and Juxtacrine Disease Drivers.Biomolecules · 2024Review
- Vascular calcification: from the perspective of crosstalk.Molecular biomedicine · 2023Review
- Article
- Pro-inflammatory mediators released by activated monocytes promote aortic valve fibrocalcific activity.Molecular medicine (Cambridge, Mass.) · 2022Article
- Uncoupling the Vicious Cycle of Mechanical Stress and Inflammation in Calcific Aortic Valve Disease.Frontiers in cardiovascular medicine · 2022Review
- Article
- The mechanistic pathways of oxidative stress in aortic stenosis and clinical implications.Theranostics · 2022Review
- LncRNA AFAP1-AS1 promotes M1 polarization of macrophages and osteogenic differentiation of valve interstitial cells.Journal of physiology and biochemistry · 2021Article
- CircRNA TGFBR2/MiR-25-3p/TWIST1 axis regulates osteoblast differentiation of human aortic valve interstitial cells.Journal of bone and mineral metabolism · 2021Article
- Inflammatory and immune checkpoint markers are associated with the severity of aortic stenosis.JTCVS open · 2021Article
- Extracellular Matrix in Calcific Aortic Valve Disease: Architecture, Dynamic and Perspectives.International journal of molecular sciences · 2021Review
- Article
- Ironing Out the Details: How Iron Orchestrates Macrophage Polarization.Frontiers in immunology · 2021Review
- Innate and adaptive immunity in cardiovascular calcification.Atherosclerosis · 2020Review
- TLR7 Expression Is Associated with M2 Macrophage Subset in Calcific Aortic Valve Stenosis.Cells · 2020Article
- Aortic Valve Stenosis and Mitochondrial Dysfunctions: Clinical and Molecular Perspectives.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe identification of the biological function of M1 macrophages and the mechanism underlying their role in valvular interstitial cell (VIC) calcification may provide therapeutic targets for the prevention of aortic valve calcification (AVC). This study investigated the mechanism by which M1 macrophages and macrophage-derived microvesicles (MVs) affected the calcification of VICs. An additional aim was to investigate the involvement of the miR-214 pathway in this process.
methodsThe M1 or M2 macrophage phenotype in human calcific aortic valve was confirmed by gene expression analysis of M1 or M2 macrophage markers. Two macrophage cell lines (BMDMs and RAW 264.7 macrophages) were transformed into M1 macrophages by lipopolysaccharide (LPS) stimulation. To investigate the mechanism by which M1 macrophages promoted VIC calcification, the generated M1 macrophages and macrophage-derived MVs were co-cultured with VICs and VICs were then used for calcification or signals analysis. In addition, a hypercholesterolemic apoE
resultsMacrophages in calcific aortic valves showed M1-directed polarization. In the VICs co-cultured with LPS-stimulated M1 macrophages and macrophage-derived MVs, VIC calcification was enhanced, and the expression of TWIST1, a direct target of miR-214, was downregulated. We showed that knockdown of TWIST1 serves as a responding molecule for miR-214 and reversed the anti-calcification action of miR-214 inhibitor, mediating signal delivery by the M1 macrophage-derived MVs to VICs and promoting VIC calcification. When M1 macrophages co-cultured with VICs, TWIST1 overexpression in M1 macrophages had no effect on the expression of TWIST1 in VICs. As shown by intravenous therapy, knockdown of miR-214 in mice seemed to improve AVC in apoE
conclusionsThese findings suggested that M1 macrophages promoted AVC by the delivery of miR-214 to valvular interstitial cells via macrophage-derived MVs and subsequent downregulation of TWIST1 of valvular interstitial cells.
Indexed as
Identifiers
28078049PMC5209529W2573972902What OpenQuestion holds
Registered trials
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