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 (674 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
A thickening and loss of elasticity of the walls of arteries that occurs with formation of atherosclerotic plaques within the arterial intima.
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: Atheroscleroses; Atherogenesis; Atherogeneses.
Where it fits in the MeSH classification
- Broader topics
- Arteriosclerosis
- Narrower topics
- Peripheral Arterial Disease
- See also
- Chylomicron Remnants; Plaque, Atherosclerotic
Related concepts
- Arteries
- Atherosclerotic Plaques
- Arterial Intima
Research landscape
PubMed indexes 67,779 records tagged with the MeSH heading “Atherosclerosis” (counts retrieved 2026-10-29). 24,186 of them (35.7%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 30,981 records.
Reviews account for 14,862 records (21.9%) and meta-analyses for 960. Randomized controlled trials number 1,812 (2.7%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,776 |
| 2000-2009 | 10,836 |
| 2010-2019 | 30,981 |
| 2020 onward | 24,186 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 14,862 | 21.9% |
| Meta-analyses | 960 | 1.4% |
| Randomized controlled trials | 1,812 | 2.7% |
Method: PubMed query "Atherosclerosis"[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 |
|---|---|---|---|---|
| ACADM-mediated fatty acid β-oxidation pathway in atherosclerosis and abdominal aortic aneurysm | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 42247143 · DOI · PMC13696078 |
| Endothelial cannabinoid CB1 receptor deficiency reduces shear stress-induced arterial inflammation and lipid uptake | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42414306 · DOI · PMC13342577 |
| Atherosclerotic Cardiovascular Disease and Cancer | 2026 | Review article Design not recorded in structured metadata | 3 | cc by PMID 42438017 · DOI · PMC13358037 |
ACADM-mediated fatty acid β-oxidation pathway in atherosclerosis and abdominal aortic aneurysm [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Background and aimsAtherosclerosis (AS) and abdominal aortic aneurysm (AAA) are both metabolism-associated vascular diseases, yet the role of lipid metabolic disturbances in their pathogenesis remains largely unknown.
- Closing excerpt
- ConclusionsThese findings define previously unrecognized distinct lipid metabolic characteristics in the pathogenesis of AS vs AAA, providing a basis for differential diagnosis and targeted treatments.
- 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 (294 words)
Background and aimsAtherosclerosis (AS) and abdominal aortic aneurysm (AAA) are both metabolism-associated vascular diseases, yet the role of lipid metabolic disturbances in their pathogenesis remains largely unknown. This study aimed to clarify the differential impact of lipid metabolic disturbances and their underlying mechanisms in AS and AAA.MethodsLipidomic analysis was performed to identify lipid metabolic differences between AS and AAA in various mouse models and different human cohorts. A multi-omics approach, integrated with functional assays, was utilized to elucidate the downstream mechanisms underlying disease-specific lipid metabolic features. Machine learning models were developed based on lipidomic features to differentiate AS from AAA.ResultsLipidomic analysis of mouse models and human samples revealed a predominant enrichment of neutral lipids (e.g. triglycerides and cholesterol esters) in AS, in contrast to phosphoglycerides in AAA. Consistently, large-scale longitudinal data from the UK Biobank showed strong positive associations of triglycerides, cholesterol, and fatty acid with the future risk of coronary atherosclerotic disease, while phosphoglycerides were negatively associated with the risk of AAA. Integrated transcriptomic and metabolomic analyses identified fatty acid metabolism, particularly Acadm-mediated fatty acid β-oxidation (FAO) pathway, as the most significantly altered lipid metabolic pathway contributing to the lipid metabolic differences between AS and AAA. Consistently, targeted restoration of the Acadm-mediated FAO pathway inhibited AS by reducing lipotoxic metabolites and preserving mitochondrial homeostasis but had little impact on AAA. Further validation with lipid droplets autophagy-tethering compound (LD·ATTEC), which selectively eliminates intracellular lipid droplets, significantly alleviated AS progression and improved FAO with no significant change observed in AAA. Finally, predictive models were developed based on lipidomic features using machine learning algorithms, facilitating accurate differentiation between these two vascular diseases.ConclusionsThese findings define previously unrecognized distinct lipid metabolic characteristics in the pathogenesis of AS vs AAA, providing a basis for differential diagnosis and targeted treatments.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42247143 · DOI · PMC13696078
Endothelial cannabinoid CB1 receptor deficiency reduces shear stress-induced arterial inflammation and lipid uptake [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Peripheral cannabinoid CB1 receptor antagonists that lack central nervous system effects are emerging as promising therapies for metabolic disease, yet the role of endothelial CB1 signaling in atherosclerosis remains unclear.
- Closing excerpt
- These findings identify endothelial CB1 as a proatherogenic, sex-biased regulator of vascular lipid transport and plaque development and associated metabolic dysfunction.
- 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 (134 words)
Peripheral cannabinoid CB1 receptor antagonists that lack central nervous system effects are emerging as promising therapies for metabolic disease, yet the role of endothelial CB1 signaling in atherosclerosis remains unclear. Here, we show that endothelial CB1 is expressed in human atherosclerotic plaques, is induced by oscillatory shear stress in atheroprone flow regions, and promotes vascular inflammation, permeability and lipid uptake. Endothelial-specific Cnr1 deletion or peripheral CB1 antagonism in mice attenuates atherosclerosis, reduces endothelial caveolae-dependent low-density lipoprotein uptake by downregulating caveolin-1 and ALK1 expression, and improves metabolic parameters in brown and white adipose tissue and the liver. The anti-atherogenic and metabolic effects are more pronounced in females, which is possibly linked to estrogen signaling. These findings identify endothelial CB1 as a proatherogenic, sex-biased regulator of vascular lipid transport and plaque development and associated metabolic dysfunction.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42414306 · DOI · PMC13342577
Atherosclerotic Cardiovascular Disease and Cancer [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Atherosclerotic cardiovascular disease (ASCVD) and cancer are increasingly recognized as interconnected diseases linked by shared immune mechanisms rather than merely overlapping risk factors.
- Closing excerpt
- This review integrates emerging mechanistic and clinical evidence and outlines how immune-based stratification and targeted modulation of inflammation may enable more precise management of patients at the intersection of cardiovascular disease and cancer.
- 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 (246 words)
Atherosclerotic cardiovascular disease (ASCVD) and cancer are increasingly recognized as interconnected diseases linked by shared immune mechanisms rather than merely overlapping risk factors. Common exposures such as smoking, obesity, diabetes, and dyslipidemia, together with aging and clonal hematopoiesis of indeterminate potential (CHIP), establish a chronic inflammatory milieu that drives both pathologies through coordinated reprogramming of myeloid and lymphoid compartments. Within this framework, a forward cardio-oncology axis is increasingly recognized, in which cancer therapies including chemotherapies, radiation, and immune checkpoint inhibitors induce cardiovascular injury, manifesting as cardiomyopathy, accelerated atherosclerosis, and immune-mediated myocarditis. Complementing this, a reverse axis has emerged in which cardiovascular injury states such as myocardial infarction, ischemia, and heart failure actively promote cancer initiation and progression through hematopoietic remodeling, extracellular vesicle-mediated communication, cardiac-derived factors, and immunosuppressive myeloid bias. At the tissue level, immune checkpoint pathways including PD-1, PD-L1, CTLA-4, LAG-3, and TIM-3 form spatially organized regulatory networks within atherosclerotic plaques. Their therapeutic perturbation restores T cell activity but may disrupt local immune homeostasis and promote plaque instability. In parallel, inflammatory cytokines such as IL-1β, IL-6, and TNF-α, often amplified by CHIP-associated clones, provide a mechanistic bridge linking atherogenesis with tumor immune evasion. Together, these observations support a unified view of ASCVD and cancer as immune-driven diseases connected by bidirectional axes of interaction. This review integrates emerging mechanistic and clinical evidence and outlines how immune-based stratification and targeted modulation of inflammation may enable more precise management of patients at the intersection of cardiovascular disease and cancer.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42438017 · DOI · PMC13358037
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 Prevalence of Familial Hypercholesterolemia Among the General Population and Patients With Atherosclerotic Cardiovascular Disease: A Systematic Review and Meta-Analysis [4]
- Research article Meta-Analysis of Leukocyte Diversity in Atherosclerotic Mouse Aortas [5]
- Research article Triglyceride-glucose index and the incidence of atherosclerotic cardiovascular diseases: a meta-analysis of cohort studies [6]
- Research article Effect of statin therapy on muscle symptoms: an individual participant data meta-analysis of large-scale, randomised, double-blind trials [7]
- Research article Integrative single-cell meta-analysis reveals disease-relevant vascular cell states and markers in human atherosclerosis [8]
- Research article Glucose-lowering drugs or strategies, atherosclerotic cardiovascular events, and heart failure in people with or at risk of type 2 diabetes: an updated systematic review and meta-analysis of randomised cardiovascular outcome trials [9]
References
- Zhang H, Sun L, Xu T, Hou X, Zhong F, Shi F, et al.. ACADM-mediated fatty acid β-oxidation pathway in atherosclerosis and abdominal aortic aneurysm. . 2026. PMID 42247143 · DOI · PMC13696078
- Chen B, Prabhu A, Li G, Kaltenbach A, Wang Y, Shakir G, et al.. Endothelial cannabinoid CB1 receptor deficiency reduces shear stress-induced arterial inflammation and lipid uptake. . 2026. PMID 42414306 · DOI · PMC13342577
- Amend A, Horstmann H, Lavine KJ, Giannarelli C, Moore KJ. Atherosclerotic Cardiovascular Disease and Cancer. . 2026. PMID 42438017 · DOI · PMC13358037
- Hu P, Dharmayat KI, Stevens CAT, Sharabiani MTA, Jones RS, Watts GF, et al.. Prevalence of Familial Hypercholesterolemia Among the General Population and Patients With Atherosclerotic Cardiovascular Disease: A Systematic Review and Meta-Analysis. Circulation. 2020. PMID 32468833 · DOI
- Zernecke A, Winkels H, Cochain C, Williams JW, Wolf D, Soehnlein O, et al.. Meta-Analysis of Leukocyte Diversity in Atherosclerotic Mouse Aortas. Circ Res. 2020. PMID 32673538 · DOI · PMC7371244
- Ding X, Wang X, Wu J, Zhang M, Cui M. Triglyceride-glucose index and the incidence of atherosclerotic cardiovascular diseases: a meta-analysis of cohort studies. Cardiovasc Diabetol. 2021. PMID 33812373 · DOI · PMC8019501
- Cholesterol Treatment Trialists' Collaboration. Effect of statin therapy on muscle symptoms: an individual participant data meta-analysis of large-scale, randomised, double-blind trials. Lancet. 2022. PMID 36049498 · DOI · PMC7613583
- Mosquera JV, Auguste G, Wong D, Turner AW, Hodonsky CJ, Alvarez-Yela AC, et al.. Integrative single-cell meta-analysis reveals disease-relevant vascular cell states and markers in human atherosclerosis. Cell Rep. 2023. PMID 37950869 · DOI · PMC12335892
- Ghosh-Swaby OR, Goodman SG, Leiter LA, Cheng A, Connelly KA, Fitchett D, et al.. Glucose-lowering drugs or strategies, atherosclerotic cardiovascular events, and heart failure in people with or at risk of type 2 diabetes: an updated systematic review and meta-analysis of randomised cardiovascular outcome trials. Lancet Diabetes Endocrinol. 2020. PMID 32333878 · 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.