ReviewCells2022
Endothelial-to-Mesenchymal Transition in Atherosclerosis: Friend or Foe?
Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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
15 citing papers in PubMed, 25 citations in OpenAlex.
- Inflammasome inhibition in myocardial infarction reduces early reperfusion injury and suppresses systemic plaque activation.Atherosclerosis · 2026Article
- Dual Lineage Tracing Identifies Cellular Mechanisms Underlying Radiation-Associated Changes in Atherosclerotic Lesion Composition-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Integrative single-cell analysis reveals endothelial diversity in the vasa vasorum of human atherosclerosis.Communications biology · 2026Article
- Oscillatory shear stress-driven endothelial-to-mesenchymal transition: a critical mechanical signal transduction mechanism in atherosclerosis progression.Cell death discovery · 2026Review
- A fibroblast-like endothelial cell state promotes atherosclerosis via C/EBPβ-activated TGF-β signaling.The EMBO journal · 2026Article
- A guide to cell-type-specific Cre mouse models in atherosclerosis: from background strains to future directions.Frontiers in cardiovascular medicine · 2026Review
- Single-cell RNA sequencing reveals sex differences in the subcellular composition and associated gene-regulatory network activity of human carotid plaques.Nature cardiovascular research · 2025Article
- Overexpression of ABCA1 in Carotid Endothelium of Hyperlipidemic Rabbits Modulates Vascular Inflammation.Human gene therapy · 2025Article
- PIM1 instigates endothelial-to-mesenchymal transition to aggravate atherosclerosis.Theranostics · 2025Article
- Review
- Article
- Single cell 'omic profiles of human aortic endothelial cellsbioRxiv : the preprint server for biology · 2024Article
- Unraveling the Role of Sex in Endothelial Cell Dysfunction: Evidence From Lineage Tracing Mice and Cultured Cells.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Cells in Atherosclerosis: Focus on Cellular Senescence from Basic Science to Clinical Practice.International journal of molecular sciences · 2023Review
- New Concepts on the Pathophysiology of Acute Coronary Syndrome.Reviews in cardiovascular medicine · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Despite many decades of research, complications of atherosclerosis resulting from the rupture or erosion of unstable plaques remain the leading cause of death worldwide. Advances in cellular lineage tracing techniques have allowed researchers to begin investigating the role of individual cell types in the key processes regulating plaque stability, including maintenance of the fibrous cap, a protective collagen-rich structure that underlies the endothelium. This structure was previously thought to be entirely derived from smooth muscle cells (SMC), which migrated from the vessel wall. However, recent lineage tracing studies have identified endothelial cells (EC) as an essential component of this protective barrier through an endothelial-to-mesenchymal transition (EndoMT), a process that has previously been implicated in pulmonary, cardiac, and kidney fibrosis. Although the presence of EndoMT in atherosclerotic plaques has been shown by several laboratories using EC-lineage tracing mouse models, whether EndoMT is detrimental (i.e., worsening disease progression) or beneficial (i.e., an athero-protective response that prevents plaque instability) remains uncertain as there are data to support both possibilities, which will be further discussed in this review.
Indexed as
Identifiers
What 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.