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Related Experiment Video

Updated: Jan 9, 2026

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

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

Published on: February 15, 2022

Smooth muscle cell phenotypic modulation during atherosclerosis.

Louise Frausto¹, Matthew L Scott², A Wayne Orr³

¹Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center at Shreveport, Shreveport, LA, USA.

Vascular Pharmacology

|December 5, 2025

Summary

Vascular smooth muscle cells (vSMCs) change phenotypes during atherosclerosis, driven by molecular and mechanical factors. This plasticity impacts plaque stability and offers therapeutic targets for vulnerable plaques.

Keywords:

Atherosclerosis Extracellular matrix Mechanotransduction Phenotypic modulation Plaque instability Vascular smooth muscle cells

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Last Updated: Jan 9, 2026

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Isolation of Murine Coronary Vascular Smooth Muscle Cells

Isolation of Murine Coronary Vascular Smooth Muscle Cells

Published on: May 30, 2016

Area of Science:

Cardiovascular Biology
Cellular Biology
Atherosclerosis Research

Background:

Vascular smooth muscle cells (vSMCs) are crucial for vascular tone and integrity in healthy arteries.
During atherosclerosis, vSMCs undergo phenotypic modulation, contributing to plaque development and instability.
Key factors driving these changes include lipid accumulation, inflammation, growth factors, and mechanical stress.

Purpose of the Study:

To review the molecular, mechanical, and post-transcriptional mechanisms governing vSMC phenotypic modulation in atherosclerosis.
To highlight the role of these mechanisms in plaque progression and vulnerability.
To discuss emerging therapeutic strategies targeting vSMC plasticity.

Main Methods:

Review of existing literature on vSMC biology in atherosclerosis.
Analysis of molecular signaling pathways (SRF-myocardin, KLF4, PDGF, TNFα, TGFβ).
Examination of mechanotransduction pathways (integrins, RhoA/ROCK, FAK, YAP/TAZ) and their role in phenotypic shifts.

Main Results:

vSMC phenotypic plasticity involves downregulation of contractile genes and induction of synthetic, inflammatory, or osteogenic phenotypes.
Mechanotransduction pathways reinforce phenotypic changes, contributing to plaque features like fibrous cap thinning and necrotic core expansion.
Non-coding RNAs fine-tune vSMC modulation, influencing plaque architecture and vulnerability.

Conclusions:

vSMC phenotypic modulation is a central process in atherosclerosis, driven by diverse molecular and mechanical cues.
Understanding these mechanisms is critical for identifying therapeutic targets to stabilize atherosclerotic plaques.
Targeting vSMC plasticity offers potential strategies to combat cardiovascular disease progression.