Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (574 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Thickening and loss of elasticity of the walls of arteries of all sizes. There are many forms classified by the types of lesions and arteries involved, such as atherosclerosis with fatty lesions in the arterial intima of medium and large muscular arteries.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Arterioscleroses.
Where it fits in the MeSH classification
- Broader topics
- Arterial Occlusive Diseases
- Narrower topics
- Arteriolosclerosis; Arteriosclerosis Obliterans; Atherosclerosis; Coronary Artery Disease; Intracranial Arteriosclerosis; Penetrating Atherosclerotic Ulcer
- See also
- Diet, Atherogenic; Atherectomy; Embolism, Cholesterol
Related concepts
- Arteries
- Atherosclerosis
- Arterial Intima
Research landscape
PubMed indexes 221,076 records tagged with the MeSH heading “Arteriosclerosis” (counts retrieved 2026-10-29). 49,977 of them (22.6%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 69,671 records.
Reviews account for 40,379 records (18.3%) and meta-analyses for 3,743. Randomized controlled trials number 7,622 (3.4%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 56,063 |
| 2000-2009 | 45,365 |
| 2010-2019 | 69,671 |
| 2020 onward | 49,977 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 40,379 | 18.3% |
| Meta-analyses | 3,743 | 1.7% |
| Randomized controlled trials | 7,622 | 3.4% |
Method: PubMed query "Arteriosclerosis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cardiovascular medicine
Cardiovascular medicine has an unusually large body of randomized trials, so the type of outcome matters: hard clinical events such as death, heart attack and stroke carry more weight than changes in blood pressure, cholesterol or imaging markers that only predict risk. Observational studies can show associations but are confounded by age, lifestyle and other illness. Check whether a result is about prevention or treatment, the baseline risk of participants, and the absolute rather than only the relative size of any benefit.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Spectral biophysical cytometry with nanosensors reveals remodelling of immune cells in atherosclerosis | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42562877 · DOI · PMC13569417 |
| Artery tertiary lymphoid organs encode a pathogenic high-affinity autoantibody-autoantigen pair in atherosclerosis | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42706439 · DOI · PMC13561875 |
| Polycomb Repressive Complex 2 drives flow-sensitive endothelial states underlying vascular inflammation and disease | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42673460 · DOI · PMC13552879 |
Spectral biophysical cytometry with nanosensors reveals remodelling of immune cells in atherosclerosis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The biophysical properties of cells determine cellular physiology.
- Closing excerpt
- Importantly, SBC achieves rapid, label-efficient profiling using commercially available instrumentation, enabling scalable biomarker discovery directly from blood samples and establishing a powerful strategy for linking biophysical phenotypes to immune cell function.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (199 words)
The biophysical properties of cells determine cellular physiology. Leveraging these properties for biomedical applications demands the ability to measure multiple parameters simultaneously across millions of cells and diverse cell types. However, current technologies are limited by throughput and low dimensionality. Here we introduce spectral biophysical cytometry (SBC), a high-throughput platform that integrates environment-sensitive nanosensors with spectral flow cytometry to resolve multiparametric biophysical properties of immune cells at single-cell resolution. By using fluorescent nanosensors that report membrane order, mitochondrial potential and membrane potential, SBC enables simultaneous quantification of key cellular physical states across diverse immune cell populations. When applied to peripheral blood mononuclear cells, SBC reveals cell-type-specific biophysical heterogeneity and identifies distinct remodelling signatures associated with atherosclerosis. In particular, T-cell subsets exhibit substantial alterations in membrane order and mitochondrial depolarization, reflecting coordinated changes in lipid composition and metabolic pathways. Integration with lipidomics and transcriptomics demonstrates that the nanosensors can detect biophysical shifts that correlate with dysregulated lipid metabolism and mitochondrial function, providing mechanistic insight into immune dysfunction in disease. Importantly, SBC achieves rapid, label-efficient profiling using commercially available instrumentation, enabling scalable biomarker discovery directly from blood samples and establishing a powerful strategy for linking biophysical phenotypes to immune cell function.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42562877 · DOI · PMC13569417
Artery tertiary lymphoid organs encode a pathogenic high-affinity autoantibody-autoantigen pair in atherosclerosis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Artery tertiary lymphoid organs (ATLOs) emerge in atherosclerosis, which is a chronic inflammatory artery disease with an autoimmune component.
- Closing excerpt
- We suggest that ATLOs harbor a dysregulated immune tolerance environment permissive for autoreactive B cells that express pathogenic autoantibodies promoting atherosclerosis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (163 words)
Artery tertiary lymphoid organs (ATLOs) emerge in atherosclerosis, which is a chronic inflammatory artery disease with an autoimmune component. However, whether disease-relevant autoimmune B cells emerge in ATLOs remains unknown. In this study, we isolate germinal center (GC) B cells from ATLOs and lymph nodes from healthy and atherosclerosis-burdened mice, expression clone 60 autoantibodies and screen them for arterial wall reactivity. ATLO GC B cell-derived autoantibodies skew to atherosclerosis-relevant autoantigens versus their counterparts in lymph nodes of both genotypes. One ATLO GC B cell-derived autoantibody (termed A6) binds to histone 2B (H2B) with high affinity. Both vaccination with H2B and adoptive transfer of A6 accelerate atherosclerosis, revealing a pathogenic autoantibody-autoantigen pair. Mechanistically, ATLOs specifically show both distorted B cell activation and immune tolerance checkpoint-regulating gene expression profiles. In a human cohort, circulating anti-H2B antibody titers positively correlate with aortic calcification in humans. We suggest that ATLOs harbor a dysregulated immune tolerance environment permissive for autoreactive B cells that express pathogenic autoantibodies promoting atherosclerosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42706439 · DOI · PMC13561875
Polycomb Repressive Complex 2 drives flow-sensitive endothelial states underlying vascular inflammation and disease [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Atherosclerotic cardiovascular disease (ASCVD), the leading cause of mortality worldwide, is driven by endothelial cell (EC) inflammatory activation and counterbalanced by protective mechanosensitive transcription factors Klf2 and Klf4 (Klf2/4).
- Closing excerpt
- This study elucidates a fundamental epigenetic mechanism in vascular inflammation and suggests a potential treatment for advanced and chronic cardiovascular inflammatory diseases.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (212 words)
Atherosclerotic cardiovascular disease (ASCVD), the leading cause of mortality worldwide, is driven by endothelial cell (EC) inflammatory activation and counterbalanced by protective mechanosensitive transcription factors Klf2 and Klf4 (Klf2/4). Plaques initiate in arterial curves or branches where disturbed shear stress (DSS) restrains Klf2/4 expression and promotes inflammatory activation of the endothelium. Importantly, DSS determines plaque vulnerability to rupture, the event that precipitates heart attack or stroke in advanced disease. However, the central determinants of endothelial inflammatory mechanotransduction and their interventional targeting to treat ASCVD pathology remain underexplored. Here, we identify Polycomb Repressive Complex (PRC) 2 as a potent, therapeutically targetable driver of vascular endothelial inflammation and ASCVD progression. PRC2 trimethylates Histone H3 Lysine27 in gene promoters/enhancers, including Klf2/4, to block gene transcription. Integrated mechanistic computation and experimental studies identified PRC2 as a central determinant of the EC state transition to inflammatory activation. PRC2 activity is elevated in endothelium from human ASCVD lesions. In murine models of acute and chronic vascular inflammation, interventional treatment with tazemetostat, a Federal Drug Administration (FDA)-approved inhibitor of the PRC2 methyltransferase EZH2, reduced endothelial inflammatory genes, slowed disease progression, and drastically improved markers of plaque stability. This study elucidates a fundamental epigenetic mechanism in vascular inflammation and suggests a potential treatment for advanced and chronic cardiovascular inflammatory diseases.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42673460 · DOI · PMC13552879
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Atherogenic index of plasma and coronary artery disease: a systematic review and meta-analysis of observational studies [4]
- Research article Clopidogrel versus aspirin for secondary prevention of coronary artery disease: a systematic review and individual patient data meta-analysis [5]
- Research article Colchicine for secondary prevention of vascular events: a meta-analysis of trials [6]
- Research article Anticoagulation and Antiplatelet Therapy for Atrial Fibrillation and Stable Coronary Disease: Meta-Analysis of Randomized Trials [7]
- Research article P2Y12 inhibitor or aspirin after percutaneous coronary intervention: individual patient data meta-analysis of randomised clinical trials [8]
- Research article Environmental risk factors for all-cause dementia, Alzheimer's disease dementia, vascular dementia, and mild cognitive impairment: An umbrella review and meta-analysis [9]
References
- Gurdap CO, Aydos D, Andronico LA, Tóth G, Ceker T, Cowgill J, et al.. Spectral biophysical cytometry with nanosensors reveals remodelling of immune cells in atherosclerosis. . 2026. PMID 42562877 · DOI · PMC13569417
- Zhang C, Zhang X, Ran Y, Wang Z, Li L, Wang S, et al.. Artery tertiary lymphoid organs encode a pathogenic high-affinity autoantibody-autoantigen pair in atherosclerosis. . 2026. PMID 42706439 · DOI · PMC13561875
- Joshi D, Rukhlenko O, Chakraborty R, Tuliakova A, Sun Z, Bhogale T, et al.. Polycomb Repressive Complex 2 drives flow-sensitive endothelial states underlying vascular inflammation and disease. . 2026. PMID 42673460 · DOI · PMC13552879
- Assempoor R, Daneshvar MS, Taghvaei A, Abroy AS, Azimi A, Nelson JR, et al.. Atherogenic index of plasma and coronary artery disease: a systematic review and meta-analysis of observational studies. Cardiovasc Diabetol. 2025. PMID 39844262 · DOI · PMC11756160
- Valgimigli M, Choi KH, Giacoppo D, Gragnano F, Kimura T, Watanabe H, et al.. Clopidogrel versus aspirin for secondary prevention of coronary artery disease: a systematic review and individual patient data meta-analysis. Lancet. 2025. PMID 40902613 · DOI
- d'Entremont MA, Poorthuis MHF, Fiolet ATL, Amarenco P, Boczar KE, Buysschaert I, et al.. Colchicine for secondary prevention of vascular events: a meta-analysis of trials. Eur Heart J. 2025. PMID 40314334 · DOI
- Rashedi S, Keykhaei M, Sato A, Steg PG, Piazza G, Eikelboom JW, et al.. Anticoagulation and Antiplatelet Therapy for Atrial Fibrillation and Stable Coronary Disease: Meta-Analysis of Randomized Trials. J Am Coll Cardiol. 2025. PMID 39918465 · DOI
- Giacoppo D, Gragnano F, Watanabe H, Kimura T, Kang J, Park KW, et al.. P2Y12 inhibitor or aspirin after percutaneous coronary intervention: individual patient data meta-analysis of randomised clinical trials. BMJ. 2025. PMID 40467090 · DOI · PMC12135077
- Jones A, Ali MU, Mayhew A, Aryal K, Correia RH, Dash D, et al.. Environmental risk factors for all-cause dementia, Alzheimer's disease dementia, vascular dementia, and mild cognitive impairment: An umbrella review and meta-analysis. Environ Res. 2025. PMID 39889875 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.