ReviewAntioxidants (Basel, Switzerland)2021
Phenotypic Modulation of Macrophages and Vascular Smooth Muscle Cells in Atherosclerosis-Nitro-Redox Interconnections.
Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- The Effect ofNutrients · 2022Pooled it
- Review
- Selective vulnerability of cerebral vasculature toScience advances · 2026Article
- Inhibition of smooth muscle phenotypic modulation by bardoxolone methyl, omaveloxolone, and cinnamaldehyde is Nrf-2 dependent.Advances in redox research · 2026Article
- Pathology-tailored nanotherapy via Galectin-3-targeted and triple-responsive nanoparticles enables multimodal therapy against aortic dissection.Journal of nanobiotechnology · 2026Article
- Decoding atherosclerosis through lactylation: multi-omics integration with experimental validation.Frontiers in cell and developmental biology · 2026Article
- Vascular Smooth Muscle-Secreted Exosomal X26nt Impedes Atherosclerosis Progression via the c-FOS/XBP1/SOD1 Axis.Immunity, inflammation and disease · 2025Article
- Oxidative stress in vascular surgical diseases: mechanisms, impacts and therapeutic perspectives.Frontiers in pharmacology · 2025Review
- Eicosapentaenoic acid induces macrophage Mox polarization to prevent diabetic cardiomyopathy.EMBO reports · 2024Article
- The two coin sides of bacterial extracellular membrane nanovesicles: atherosclerosis trigger or remedy.Discover nano · 2024Review
- Article
- Association of nitric oxide levels and lipid profile with endothelial dysfunction in type 2 diabetic patients.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2024Article
- Glucagon-like peptide-1 receptor agonists: new strategies and therapeutic targets to treat atherosclerotic cardiovascular disease.Frontiers in pharmacology · 2024Review
- MicroRNA regulation of phenotypic transformations in vascular smooth muscle: relevance to vascular remodeling.Cellular and molecular life sciences : CMLS · 2023Review
- Cellular FXIII in Human Macrophage-Derived Foam Cells.International journal of molecular sciences · 2023Article
- Cellular mechanisms and molecular pathways linking bitter taste receptor signalling to cardiac inflammation, oxidative stress, arrhythmia and contractile dysfunction in heart diseases.Inflammopharmacology · 2023Review
- Extracellular vesicles in atherosclerosis and vascular calcification: the versatile non-coding RNAs from endothelial cells and vascular smooth muscle cells.Frontiers in medicine · 2023Review
- miR-33a Expression Attenuates ABCA1-Dependent Cholesterol Efflux and Promotes Macrophage-Like Cell Transdifferentiation in Cultured Vascular Smooth Muscle Cells.Journal of lipids · 2023Article
- Targeting the Crosstalk of Immune Response and Vascular Smooth Muscle Cells Phenotype Switch for Arteriovenous Fistula Maturation.International journal of molecular sciences · 2022Article
- Partial Synthetic PPARƳ Derivative Ameliorates Aorta Injury in Experimental Diabetic Rats Mediated by Activation of miR-126-5p Pi3k/AKT/PDK 1/mTOR Expression.Pharmaceuticals (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Monocytes/macrophages and vascular smooth muscle cells (vSMCs) are the main cell types implicated in atherosclerosis development, and unlike other mature cell types, both retain a remarkable plasticity. In mature vessels, differentiated vSMCs control the vascular tone and the blood pressure. In response to vascular injury and modifications of the local environment (inflammation, oxidative stress), vSMCs switch from a contractile to a secretory phenotype and also display macrophagic markers expression and a macrophagic behaviour. Endothelial dysfunction promotes adhesion to the endothelium of monocytes, which infiltrate the sub-endothelium and differentiate into macrophages. The latter become polarised into M1 (pro-inflammatory), M2 (anti-inflammatory) or Mox macrophages (oxidative stress phenotype). Both monocyte-derived macrophages and macrophage-like vSMCs are able to internalise and accumulate oxLDL, leading to formation of "foam cells" within atherosclerotic plaques. Variations in the levels of nitric oxide (NO) can affect several of the molecular pathways implicated in the described phenomena. Elucidation of the underlying mechanisms could help to identify novel specific therapeutic targets, but to date much remains to be explored. The present article is an overview of the different factors and signalling pathways implicated in plaque formation and of the effects of NO on the molecular steps of the phenotypic switch of macrophages and vSMCs.
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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 Socratic graph.