ArticleJCI insight2023
CD163+ macrophages restrain vascular calcification, promoting the development of high-risk plaque.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 30 citations in OpenAlex.
- A single-center observational study on the impact of intravascular ultrasound-detected attenuated plaque on coronary microvascular dysfunction following percutaneous coronary intervention.The international journal of cardiovascular imaging · 2026Observational
- Artery tertiary lymphoid organs, neuro-immune interaction and their mediators in atherosclerosis.Basic research in cardiology · 2026Review
- Serum sCD163 indicates disease severity and prognosis in sudden sensorineural hearing loss.Molecular medicine (Cambridge, Mass.) · 2026Article
- Review
- VSMCs and the immune microenvironment: a multidimensional regulatory network driving vascular injury and repair.Frontiers in immunology · 2026Review
- Iron in Vascular Calcification: Pro-Calcific Agent or Protective Modulator?International journal of molecular sciences · 2025Review
- Identification of crucial genes for polycystic ovary syndrome and atherosclerosis through comprehensive bioinformatics analysis and machine learning.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2025Article
- Six-Month Patency of Long Carotid Bypass Grafts Constructed with In-Body Tissue Architecture-Induced Small-Diameter Biotubes in a Goat Model.Bioengineering (Basel, Switzerland) · 2025Article
- Fucosylated haptoglobin promotes inflammation via Mincle in sepsis: an observational study.Nature communications · 2025Observational
- Clinical application and immune infiltration landscape of stemness-related genes in heart failure.ESC heart failure · 2025Article
- The role of macrophages in vascular calcification: strategies for diagnosis and treatment.Frontiers in immunology · 2025Review
- Chitosan-Based Nanoparticles Targeted Delivery System: In Treatment Approach for Dyslipidemia.International journal of nanomedicine · 2025Review
- Macrophages as key modulators of calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025Review
- Spatial Transcriptomic Approach to Understanding Coronary Atherosclerotic Plaque Stability.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- HIV persists in late coronary atheroma and is associated with increased local inflammation and disease progression.Research square · 2024Article
- Oral Nanoformulations in Cardiovascular Medicine: Advances in Atherosclerosis Treatment.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Inflammatory Biomarkers to Predict Major Adverse Cardiovascular Events in Patients with Carotid Artery Stenosis.Medicina (Kaunas, Lithuania) · 2024Article
- Development of a CD163-Targeted PET Radiotracer That Images Resident Macrophages in Atherosclerosis.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2024Article
- The interplay of collagen, macrophages, and microcalcification in atherosclerotic plaque cap rupture mechanics.Basic research in cardiology · 2024Review
- Differential expression of Semaphorin-7A /CD163-positive macrophages in large artery and cardiogenic stroke.BMC neurology · 2024Article
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37 authors at 5 institutions in 2 countries.
Funding
Abstract
Vascular calcification (VC) is concomitant with atherosclerosis, yet it remains uncertain why rupture-prone high-risk plaques do not typically show extensive calcification. Intraplaque hemorrhage (IPH) deposits erythrocyte-derived cholesterol, enlarging the necrotic core and promoting high-risk plaque development. Pro-atherogenic CD163+ alternative macrophages engulf hemoglobin:haptoglobin (HH) complexes at IPH sites. However, their role in VC has never been examined to our knowledge. Here we show, in human arteries, the distribution of CD163+ macrophages correlated inversely with VC. In vitro experiments using vascular smooth muscle cells (VSMCs) cultured with HH-exposed human macrophage - M(Hb) - supernatant reduced calcification, while arteries from ApoE-/- CD163-/- mice showed greater VC. M(Hb) supernatant-exposed VSMCs showed activated NF-κB, while blocking NF-κB attenuated the anticalcific effect of M(Hb) on VSMCs. CD163+ macrophages altered VC through NF-κB-induced transcription of hyaluronan synthase (HAS), an enzyme that catalyzes the formation of the extracellular matrix glycosaminoglycan, hyaluronan, within VSMCs. M(Hb) supernatants enhanced HAS production in VSMCs, while knocking down HAS attenuated its anticalcific effect. NF-κB blockade in ApoE-/- mice reduced hyaluronan and increased VC. In human arteries, hyaluronan and HAS were increased in areas of CD163+ macrophage presence. Our findings highlight an important mechanism by which CD163+ macrophages inhibit VC through NF-κB-induced HAS augmentation and thus promote the high-risk plaque development.
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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.