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Endothelial to mesenchymal transition (EndMT) is a dynamic and reversible cellular process in which endothelial cells lose their vascular identity and acquire mesenchymal characteristics such as enhanced motility, contractility and extracellular matrix production.
EndMT is increasingly recognized as a central mechanism linking vascular dysfunction, organ fibrosis and tumor microenvironment remodeling in chronic diseases.
During EndMT, endothelial cells:
EndMT plays essential roles in:
EndMT represents a critical mechanism of vascular plasticity in both physiological and pathological contexts.
EndMT activity can be efficiently assessed by measuring gene expression changes in:
Gene expression profiling provides a quantitative and reproducible approach to characterize endothelial plasticity and mesenchymal transition dynamics across experimental models.
EndMT biomarker list
View the genes included in our EndMT-related qPCR arrays.
Transcriptional
regulation
EndMT is controlled by master transcription factors:
These factors repress endothelial genes and activate mesenchymal gene programs.
Loss of endothelial
identity
Key endothelial markers that decrease during EndMT:
This leads to endothelial barrier dysfunction and increased permeability.
Acquisition of mesenchymal
phenotype
Mesenchymal markers that increase:
This transition promotes contractility, matrix deposition and tissue stiffening.
EndMT integrates multiple extracellular signals:
Primary inducer of EndMT via SMAD-dependent and SMAD-independent pathways.
Enhances mesenchymal gene expression and synergizes with TGF-β signaling.
Regulates endothelial plasticity through Snail and Twist activation.
Supports survival and mesenchymal transition.
HIF activation and ROS signaling promote EndMT in fibrosis and cancer.
TNF-α and IL-1 disrupt endothelial junctions and reinforce mesenchymal traits.
Fibrosis
EndMT contributes to fibroblast accumulation and extracellular matrix production in:
Persistent EndMT promotes organ dysfunction.
Cardiovascular Diseases
In atherosclerosis and vascular remodeling, EndMT leads to:
Pulmonary Hypertension
EndMT contributes to vascular wall thickening and pathological remodeling.
Cancer
Within the tumor microenvironment, EndMT:
Understanding this endothelial plasticity mechanism at the molecular level is essential for:
Robust biomarker profiling ensures reproducible quantification of endothelial–mesenchymal transition dynamics and supports translational research applications.
AnyGenes® provides validated qPCR pathway arrays and fully customizable SignArrays® dedicated to EndMT research in:
Our solutions enable researchers to:
Scientific data is only as powerful as the analysis behind it.
AnyGenes® provides a dedicated data analysis tool specifically developed for SignArrays® pathway panels.
What does it allow you to do?
Developed on Excel (compatible with 2007+), the software is user-friendly and requires no advanced bioinformatics skills.
Customize your own signaling pathways (SignArrays®) with the factors of your choice!
Simply download and complete our Personalized SignArrays® information file
and send it at
[email protected]
to initiate your project.
This endothelial transition process is a reversible cellular process in which endothelial cells lose vascular markers and acquire mesenchymal characteristics such as increased motility, contractility and extracellular matrix production.
EndMT is primarily induced by TGF-β signaling and can be reinforced by Wnt/β-catenin, Notch, PI3K-AKT, inflammatory cytokines, hypoxia and oxidative stress.
In fibrotic diseases, EndMT contributes to fibroblast accumulation and excessive extracellular matrix deposition, promoting organ stiffening and dysfunction.
EndMT is implicated in cardiac fibrosis, pulmonary fibrosis, renal fibrosis, atherosclerosis, pulmonary hypertension and cancer progression.
EndMT activity can be assessed by measuring gene expression changes in endothelial markers (CDH5, PECAM1), mesenchymal markers (ACTA2, VIM, FN1), transcription factors (SNAI1, ZEB1, TWIST1) and pathway components using targeted qPCR arrays.
| Signaling Pathways | Product ref | Informations |
|---|---|---|
Endothelial To Mesenchymal Transition | ENDMT1H1 |
| Signaling Pathways | Product ref | Informations |
|---|---|---|
Endothelial To Mesenchymal Transition | ENDMT1M1 |
| Signaling Pathways | Product ref | Informations |
|---|---|---|
Endothelial To Mesenchymal Transition | ******* |
Biomarker list in progress. |
| Signaling Pathways | Product ref | Informations |
|---|---|---|
Endothelial To Mesenchymal Transition | ******* |
Biomarker list in progress. |
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1. Bischoff J. Endothelial-to-Mesenchymal Transition. Circ Res. (2019);124(8):1163-1165.
2. Gorelova A. Endothelial-to-Mesenchymal Transition in Pulmonary Arterial Hypertension. Antioxid Redox Signal. (2021);34(12):891-914.
3. Piera-Velazquez S, Jimenez SA. Endothelial to Mesenchymal Transition: Role in Physiology and in the Pathogenesis of Human Diseases. Physiol Rev. (2019);99(2):1281-1324.
3. Xu Y, Kovacic JC. Endothelial to Mesenchymal Transition in Health and Disease. Annu Rev Physiol. (2023);85:245-267.