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Updated: Sep 14, 2025

Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression
Published on: January 15, 2022
The new perspective on understanding the mechanisms of cardiovascular diseases development
Ulyana Khovantseva1, Diana Kiseleva2,3, Vadim Cherednichenko2
1Petrovsky National Research Center of Surgery, 119435, Moscow, Russian Federation. ulyana.khovantseva@gmail.com.
Insights
Smooth muscle cells (SMCs) in patients with cardiovascular diseases may undergo phenotypic switching, affecting vascular wall structure. This cellular change, linked to LDL internalization, may drive aneurysm development.
Area of Science:
- Vascular Biology
- Cardiovascular Research
- Cellular Biology
Background:
- Cardiovascular diseases (CVD) are a leading global cause of mortality.
- Endothelial dysfunction is a recognized factor in CVD development.
- Alternative hypotheses suggest smooth muscle cell (SMC) dysfunction drives CVD.
Purpose of the Study:
- To investigate the functional characteristics of SMCs from the human thoracic aorta in CVD patients.
- To analyze SMCs isolated from both the tunica intima and tunica media.
Main Methods:
- Isolation of SMCs from the tunica intima and tunica media of the human thoracic aorta.
- Analysis of SMCs from patients with cardiovascular diseases, including aneurysms (n=6).
Main Results:
- Phenotypic switching was observed in SMCs from patients with aneurysms.
- This switching led to extracellular matrix remodeling and impaired cellular receptor interactions.
- LDL internalization by SMCs may trigger complement-mediated phagocytosis, potentially driving aneurysm formation.
Conclusions:
- SMC phenotypic modulation is a significant factor in cardiovascular disease, particularly aneurysms.
- The study highlights potential mechanisms involving LDL, complement activation, and phagocytosis in aneurysm pathogenesis.
Abstract:
Cardiovascular diseases (CVD) are one of the leading causes of death worldwide. From a modern point of view, endothelial dysfunction is considered as a key factor leading to the development of CVD. However, scientists have suggested that the main causes of the development of CVD might be functional disorders and phenotypic modulation of smooth muscle cells (SMCs) that make up the vascular wall. In this regard, the aim of our study was to evaluate the functional features of SMCs isolated from the tunica intima and from the tunica media of the thoracic part of the human aorta in patients with CVD. In our research we showed that phenotypic switching can occur in SMCs isolated from patients with aneurysms (n = 6), resulting in remodeling of the extracellular matrix and impaired interaction between cellular receptors. In addition, it is probable that the activation of complement-mediated phagocytosis as a result of LDL internalization by SMCs might be one of the key mechanisms in the process of aneurysm development.
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