Research Highlights

Ndenda and Colleagues published a recent study, "A Mathematical Model for Smooth Muscle Cell Phenotype Switching In Atherosclerotic Plaque." The authors found that when SMCs switch to a macrophage-like phenotype, there is an increase in the lipid quantity in the model plaque that is internalised inside cells. Additionally, removal of SMCs from the model plaque via phenotype switching reduces the number of SMCs in the fibrous cap, increases the lipid in the necrotic core, and increases plaque inflammation. The model suggests that the switch of SMCs to a macrophage-like phenotype may drive the development of unstable and pathological plaques.

You can find the article in the Bulletin of Mathematical Biology here.

Yu-Yuan Zhang and Colleagues published a study in 2025, "Unveiling the Negative Synergistic Effect of Wall Shear Stress and Insulin on Endothelial NO Dynamics by Mathematical Modeling." As shown above, the study uses mathematical modeling to understand nitric oxide (NO) signaling from endothelial cells (ECs) in the setting of diabetic vascular complications. The authors use a mathematical model of NO signaling to understand how EC function, NO production, and stimulation by wall shear stress and insulin interact. The authors found that oscillatory wall shear stress contributes to NO precursors.

You can find the article in the Bulletin of Mathematical Biology here.

Dilmini Warnakulasooriya & Vladimir E. Bondarenko have published an article titled "EAD Mechanisms in Hypertrophic Mouse Ventricular Myocytes: Insights from a Compartmentalized Mathematical Model." The authors developed a mathematical model of ventricular myocytes during the early stages of transverse aortic constriction (TAC) in a mouse model. The authors use the model to compare cell in hypertropic TAC conditions to normal, health ventricular myocytes.

You can find the article in the Bulletin of Mathematical Biology here.