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On-Chip Endothelial Inflammatory Phenotyping

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Published on: July 21, 2012

Endothelial Cell Phenotypic Plasticity in Atherosclerosis.

Laura Alonso-Herranz^1,2, Julián Albarrán-Juárez³

¹Atherosclerosis Research Unit, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.

Handbook of Experimental Pharmacology

|June 18, 2026

Summary

Endothelial-to-mesenchymal transition (EndMT) drives atherosclerosis by altering vessel cells. Targeting EndMT pathways offers precision medicine strategies for cardiovascular disease, promoting plaque stabilization and vascular integrity.

Keywords:

Atherosclerosis Endothelial cell dysfunction Endothelial-to-mesenchymal transition Heterogeneity and plasticity Single-cell transcriptomics

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Area of Science:

Vascular Biology
Cellular Plasticity
Cardiovascular Disease Pathogenesis

Background:

Atherosclerosis, a major cause of death, begins with endothelial cell (EC) dysfunction and vascular remodeling.
The endothelium exhibits heterogeneity and plasticity, with endothelial-to-mesenchymal transition (EndMT) being a key process.
EndMT involves ECs losing identity and gaining pro-fibrotic traits, contributing to atherosclerotic lesion development.

Purpose of the Study:

To review how atherogenic factors trigger EndMT.
To explore signaling networks driving EndMT and counterbalancing mechanisms.
To summarize methods for studying EC plasticity and discuss therapeutic strategies.

Main Methods:

Review of in situ co-staining, genetic lineage tracing, epigenetic fate mapping, and single-cell multi-omics.
Analysis of in vitro, organ-on-a-chip, and murine models of EC plasticity.
Synthesis of evidence on atherogenic cues and signaling pathways.

Main Results:

Atherogenic cues (disturbed flow, oxidative stress, inflammation, matrix stiffening) initiate EndMT.
Convergent signaling networks (TGF-β, Wnt/β-catenin, Notch, NF-κB/STAT3, HDAC9) drive EndMT.
Protective pathways (FGF, KLF2/KLF4) maintain endothelial homeostasis.
Distinct disease-associated EC subpopulations identified through multi-omics.

Conclusions:

EndMT is a critical cellular mechanism in atherosclerosis development.
Understanding EC plasticity is key to developing targeted therapies.
Precision medicine strategies can reprogram pathogenic endothelial states for plaque stabilization and vascular health.