ReviewStem cells international2016
Endothelial Plasticity: Shifting Phenotypes through Force Feedback.
Review in Stem cells international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 73 citations in OpenAlex.
- Proteolysis at the extracellular matrix interface: Molecular architects and regulators in health and disease.The FEBS journal · 2026Review
- A new challenging dilemma to prevent major cardiovascular events in patients with chronic venous disorders.Journal of vascular surgery. Venous and lymphatic disorders · 2026Article
- Epitranscriptomic regulation of endothelial plasticity under hemodynamic forces: insights from the KLF2/4-METTL3-H19 pathway.Frontiers in genetics · 2026Review
- Article
- Vascular leakage during circulatory failure: physiopathology, impact and treatments.Annals of intensive care · 2025Review
- Macrophages as key modulators of calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025Review
- Insights into preclinical models of calcific aortic valve disease and their translational potential.Frontiers in cardiovascular medicine · 2025Review
- Review
- Metabolic reprogramming, oxidative stress, and pulmonary hypertension.Redox biology · 2023Review
- TGFβ signaling pathways in human health and disease.Frontiers in molecular biosciences · 2023Review
- Actin cytoskeleton in angiogenesis.Biology open · 2022Review
- ATF3 in atherosclerosis: a controversial transcription factor.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Peripheral vascular remodeling during ischemia.Frontiers in pharmacology · 2022Review
- Endothelial-mesenchymal transition induced by metastatic 4T1 breast cancer cells in pulmonary endothelium in aged mice.Frontiers in molecular biosciences · 2022Article
- Cytoskeleton Reorganization in EndMT-The Role in Cancer and Fibrotic Diseases.International journal of molecular sciences · 2021Review
- A narrative review of the relationship between TGF-β signaling and gynecological malignant tumor.Annals of translational medicine · 2021Review
- Endothelial-Mesenchymal Transition in Cardiovascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- The 14-3-3η/GSK-3β/β-catenin complex regulates EndMT induced by 27-hydroxycholesterol in HUVECs and promotes the migration of breast cancer cells.Cell biology and toxicology · 2021Article
- High stretch induces endothelial dysfunction accompanied by oxidative stress and actin remodeling in human saphenous vein endothelial cells.Scientific reports · 2021Article
- Modulation of EndMT by Hydrogen Sulfide in the Prevention of Cardiovascular Fibrosis.Antioxidants (Basel, Switzerland) · 2021Review
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 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The endothelial lining of the vasculature is exposed to a large variety of biochemical and hemodynamic stimuli with different gradients throughout the vascular network. Adequate adaptation requires endothelial cells to be highly plastic, which is reflected by the remarkable heterogeneity of endothelial cells in tissues and organs. Hemodynamic forces such as fluid shear stress and cyclic strain are strong modulators of the endothelial phenotype and function. Although endothelial plasticity is essential during development and adult physiology, proatherogenic stimuli can induce adverse plasticity which contributes to disease. Endothelial-to-mesenchymal transition (EndMT), the hallmark of endothelial plasticity, was long thought to be restricted to embryonic development but has emerged as a pathologic process in a plethora of diseases. In this perspective we argue how shear stress and cyclic strain can modulate EndMT and discuss how this is reflected in atherosclerosis and pulmonary arterial hypertension.
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.