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Related Experiment Video

Updated: Apr 12, 2026

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
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A Mathematical Model for Smooth Muscle Cell Phenotype Switching In Atherosclerotic Plaque.

Joseph P Ndenda1,2, Michael G Watson3, Ashish Misra4

  • 1School of Mathematics and Statistics, University of Sydney, Sydney, NSW, 2006, Australia.

Bulletin of Mathematical Biology
|April 10, 2026
PubMed
Summary
This summary is machine-generated.

Smooth muscle cells (SMCs) can transform into macrophage-like cells, increasing plaque lipid load and inflammation. This transformation drives the development of unstable atherosclerotic plaques, increasing risks for heart attacks and strokes.

Keywords:
AtherosclerosisOrdinary differential equation modelPhenotype switchSmooth muscle cell

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Area of Science:

  • Cardiovascular Biology
  • Mathematical Modeling
  • Atherosclerosis Research

Background:

  • Smooth muscle cells (SMCs) are key players in atherosclerotic plaque development.
  • SMCs can internalize lipids and undergo a phenotypic switch to a macrophage-like state.
  • This transformation influences plaque composition and stability.

Purpose of the Study:

  • To model the impact of SMC phenotypic switching on atherosclerotic plaque progression.
  • To investigate how SMC-derived macrophages (SDMs) affect plaque characteristics.
  • To understand the mechanisms driving plaque vulnerability.

Main Methods:

  • Formulation of an ordinary differential equation (ODE) model.
  • Simulation of SMC, monocyte-derived macrophage (MDM), and SDM populations.
  • Analysis of lipid load dynamics and cellular composition within the plaque model.

Main Results:

  • SMC phenotype switching increases intracellular lipid accumulation in the plaque.
  • Phenotypic switching reduces SMCs in the fibrous cap, increasing necrotic core lipid and inflammation.
  • High proliferation or reduced cell death in SDMs leads to more pathological plaques.

Conclusions:

  • SMC phenotypic switching to a macrophage-like state promotes vulnerable plaque development.
  • This cellular transformation contributes to increased plaque instability and inflammation.
  • The study highlights SMC plasticity as a critical factor in atherosclerosis progression.