ArticleThe American journal of pathology1998
Clonal architecture of normal and atherosclerotic aorta: implications for atherogenesis and vascular development.
Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.
- Review and meta-analysis of epidemiological associations between low/moderate doses of ionizing radiation and circulatory disease risks, and their possible mechanisms.Radiation and environmental biophysics · 2010Pooled it
- Vascular Smooth Muscle Cell Plasticity in Atherosclerosis: Mechanisms, Recent Advances, and Therapeutic Implications.Reviews in cardiovascular medicine · 2026Review
- Clonal Expansion in Cardiovascular Pathology.JACC. Basic to translational science · 2024Review
- Sprouty1 has a protective role in atherogenesis and modifies the migratory and inflammatory phenotype of vascular smooth muscle cells.Atherosclerosis · 2023Article
- Role of vascular smooth muscle cell clonality in atherosclerosis.Frontiers in cardiovascular medicine · 2023Review
- Mechanisms of fibrous cap formation in atherosclerosis.Frontiers in cardiovascular medicine · 2023Review
- Emerging Concepts of Vascular Cell Clonal Expansion in Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2022Review
- Macrophages in Atherosclerosis, First or Second Row Players?Biomedicines · 2021Review
- Metformin Suppresses the Progress of Diabetes-Accelerated Atherosclerosis by Inhibition of Vascular Smooth Muscle Cell Migration Through AMPK-Pdlim5 Pathway.Frontiers in cardiovascular medicine · 2021Article
- Genetics of Arterial-Wall-Specific Mechanisms in Atherosclerosis: Focus on Mitochondrial Mutations.Current atherosclerosis reports · 2020Review
- Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel.European heart journal · 2020 · on this mapArticle
- Vascular smooth muscle cells in atherosclerosis.Nature reviews. Cardiology · 2019Review
- Clonal Smooth Muscle Cell Expansion, Autophagy, and Vascular Integrity in Aortic Aneurysm Disease.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Integrin beta3 regulates clonality and fate of smooth muscle-derived atherosclerotic plaque cells.Nature communications · 2018Article
- Smooth muscle cell fate and plasticity in atherosclerosis.Cardiovascular research · 2018Review
- Lineage tracking of origin and fate of smooth muscle cells in atherosclerosis.Cardiovascular research · 2018Review
- An update on clonality: what smooth muscle cell type makes up the atherosclerotic plaque?F1000Research · 2018Review
- Diverse cellular architecture of atherosclerotic plaque derives from clonal expansion of a few medial SMCs.JCI insight · 2017Article
- Article
- Dynamic Patterns of Clonal Evolution in Tumor Vasculature Underlie Alterations in Lymphocyte-Endothelial Recognition to Foster Tumor Immune Escape.Cancer research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
X chromosome inactivation studies indicate that smooth muscle cells in human atherosclerosis are monoclonal. Monoclonality could arise either by 1) proliferation of a single cell in the adult intima, eg, by selection or mutation, or 2) proliferation of many cells within a large, pre-existing clonal patch that formed during development. To determine whether clonal expansion occurs concomitantly with plaque growth or as part of normal development, X chromosome inactivation patterns were mapped in microdissected samples of aortic smooth muscle, using the human androgen receptor locus as a marker. As expected, 43% of plaque samples were skewed toward one X chromosome, indicating a monoclonal population. Surprisingly, 25% of normal medial samples and 31% of diffuse intimal thickening samples also were skewed toward one X chromosome, indicating a relatively large patch size. Furthermore, 30% of diffuse intimal thickening and 22% of medial samples showed contiguous regions of 4 mm skewed to the same allele, showing that patch length often exceeded 4 mm. Intima and overlying media typically were skewed to the same allele (73% concordance), suggesting common cells of origin. Because patch size is large in normal arteries, X-inactivation analysis cannot discriminate between a monoclonal and a polyclonal origin of plaque smooth muscle cells. We propose that human arteries grow by expanding coherent smooth muscle clones, with little mixing of adjacent clones. Determining whether plaques arise by clonal expansion will require other approaches, such as analysis of somatic mutations; the finding of large X-inactivation patches raises the possibility that plaques arise from a pre-existing (developmental) clone.
Indexed as
Identifiers
9546352PMC1858235W1237363190What OpenQuestion holds
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 OpenQuestion graph.