ArticleAdvanced functional materials2022
Single-Cell Transcriptomic Census of Endothelial Changes Induced by Matrix Stiffness and the Association with Atherosclerosis.
Article in Advanced functional materials, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 30 citations in OpenAlex.
- Nuclear mechanotransduction: tools for mechanical perturbation and chromatin characterization.Nucleus (Austin, Tex.) · 2026Review
- Cellular Responses to Mechanical Cues Across Scales: From Fundamental Insights to Translational Potential.Advanced healthcare materials · 2026Review
- Angiogenic Potential of Endothelial Cells in Response to the Stiffness and Anisotropy of Right Ventricle Mimetic Scaffolds.Bioengineering (Basel, Switzerland) · 2026Article
- EZH2 inhibition via GSK-126 mitigates EndMT and atherosclerosis in diabetes: A translational epigenetic approach.Science advances · 2026Article
- Endothelial to mesenchymal transition in cardiovascular diseases: molecular insights and clinical perspectives.European heart journal · 2026Review
- Temporal inhibition of ADAM17 in fibroblasts reduces stiffness and promotes vascularization following myocardial infarction.Cardiovascular research · 2026Article
- Review
- The relationship between fibrinogen-to-albumin ratio and brachial-ankle pulse wave velocity in elderly individuals in China: a cross-sectional study.Frontiers in cardiovascular medicine · 2026Article
- TRPV4-Mediated Mechanosensing Regulates the Endothelial-to-Mesenchymal Transition: Implications for Atherosclerosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- COL8A1 regulates endothelial phenotype in inflammatory endothelial-to-mesenchymal transition.American journal of physiology. Heart and circulatory physiology · 2025Article
- Substrate stiffness and shear stress collectively regulate the inflammatory phenotype in cultured human brain microvascular endothelial cells.Fluids and barriers of the CNS · 2025Article
- Microenvironmental determinants of endothelial cell heterogeneity.Nature reviews. Molecular cell biology · 2025Review
- Extracellular matrix in vascular homeostasis and disease.Nature reviews. Cardiology · 2025Review
- Endothelial cell (EC)-specific Ctgf/Ccn2 expression increases EC reprogramming and atherosclerosis.Matrix biology : journal of the International Society for Matrix Biology · 2025Article
- Promising Adventitia in Atherosclerosis.Current vascular pharmacology · 2025Review
- Extracellular matrix stiffness regulates the proliferation and migration capacities of lymphatic endothelial cells via FAT1.Frontiers in cell and developmental biology · 2025Article
- Collagen VIII in vascular diseases.Matrix biology : journal of the International Society for Matrix Biology · 2024Review
- A mechanical modeling framework to study endothelial permeability.Biophysical journal · 2024Article
- Post-ischemic inactivation of HIF prolyl hydroxylases in endothelium promotes maladaptive kidney repair by inducing glycolysis.bioRxiv : the preprint server for biology · 2023Article
- Mechanosensing and Mechanosignal Transduction in Atherosclerosis.Current atherosclerosis reports · 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
10 authors at 6 institutions in 1 country.
Funding
Abstract
Vascular endothelial cell (EC) plasticity plays a critical role in the progression of atherosclerosis by giving rise to mesenchymal phenotypes in the plaque lesion. Despite the evidence for arterial stiffening as a major contributor to atherosclerosis, the complex interplay among atherogenic stimuli in vivo has hindered attempts to determine the effects of extracellular matrix (ECM) stiffness on endothelial-mesenchymal transition (EndMT). To study the regulatory effects of ECM stiffness on EndMT, an in vitro model is developed in which human coronary artery ECs are cultured on physiological or pathological stiffness substrates. Leveraging single-cell RNA sequencing, cell clusters with mesenchymal transcriptional features are identified to be more prevalent on pathological substrates than physiological substrates. Trajectory inference analyses reveal a novel mesenchymal-to-endothelial reverse transition, which is blocked by pathological stiffness substrates, in addition to the expected EndMT trajectory. ECs pushed to a mesenchymal character by pathological stiffness substrates are enriched in transcriptional signatures of atherosclerotic ECs from human and murine plaques. This study characterizes at single-cell resolution the transcriptional programs that underpin EC plasticity in both physiological or pathological milieus, and thus serves as a valuable resource for more precisely defining EndMT and the transcriptional programs contributing to atherosclerosis.
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.