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Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro

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Bridging the Translational Gap: Rethinking Smooth Muscle Cell Plasticity in Atherosclerosis Through Human-Relevant In

Liliana Som¹, Nicola Smart¹

¹Department of Physiology, Anatomy and Genetics, Institute of Developmental & Regenerative Medicine, BHF Oxford Centre of Research Excellence, University of Oxford, Oxford OX3 7TY, UK.

|December 10, 2025

Summary

This summary is machine-generated.

Human vascular smooth muscle cell (SMC) plasticity is key to atherosclerosis, but current models miss human complexity. This review highlights how advanced in vitro models, validated with human data, can bridge this knowledge gap.

Keywords:

human-relevant in vitro modelling omics phenotypic plasticity smooth muscle cell

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Area of Science:

Cardiovascular Biology
Cellular Plasticity
Atherosclerosis Research

Background:

Vascular smooth muscle cell (SMC) plasticity significantly influences atherosclerosis progression.
Existing murine models inadequately represent the diverse human SMC phenotypes relevant to disease.
A translational gap exists in understanding human SMC states due to model limitations.

Purpose of the Study:

To review and advocate for improved human in vitro models for studying SMC plasticity.
To address the limitations of current experimental models in capturing human SMC complexity.
To propose integrating advanced in vitro systems with human omics data for better disease modeling.

Main Methods:

Critical assessment of various in vitro systems, including monocultures, co-cultures, and 3D platforms.
Examination of how these systems can model human SMC plasticity.
Emphasis on benchmarking in vitro models against human single-cell and multi-omics data.

Main Results:

Human studies reveal a wider range of SMC phenotypes than currently modeled.
Advanced in vitro models offer potential for better recapitulation of human SMC plasticity.
Benchmarking against human data is crucial for validating and refining experimental models.

Conclusions:

Bridging the translational gap requires human in vitro models that critically assess and integrate omics data.
Selecting and validating models based on human data is essential for accurate atherosclerosis research.
Improved human in vitro models are necessary to fully understand SMC plasticity in human disease.