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Updated: Aug 9, 2026
Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
Connexins in atherosclerosis
Christos E Chadjichristos1, Jean-Paul Derouette, Brenda R Kwak
1Division of Cardiology, Department of Internal Medicine, University Hospital Geneva, Geneva, Switzerland.
Insights
Vascular remodeling, crucial in cardiovascular diseases like atherosclerosis and restenosis, involves cell communication. Altered connexin expression and gap junction communication are implicated in these conditions.
Area of Science:
- Cardiovascular Biology
- Cellular Communication
- Vascular Pathophysiology
Background:
- Vascular wall remodeling is central to physiological processes and cardiovascular diseases such as atherosclerosis and restenosis.
- Atherosclerosis is a leading cause of death, and restenosis post-angioplasty is a significant clinical issue.
- Cytokines and growth factors are critical in the complex interactions driving atherosclerosis and restenosis.
Purpose of the Study:
- To summarize evidence supporting the role of gap-junction-mediated intercellular communication in vascular diseases.
- To investigate alterations in vascular connexin patterns during disease development.
- To explore the impact of disturbed flow, inflammation, and smooth muscle cell activation on connexin expression.
Main Methods:
- Review of existing evidence on gap junction communication in vascular diseases.
- Analysis of connexin expression patterns in atherosclerotic plaques and restenosis.
- Examination of the effects of physiological and pathological stimuli on connexin expression.
- Evaluation of genetically modified connexin expression in mouse models of vascular disease.
Main Results:
- Connexin patterns are altered during atherosclerotic plaque formation and restenosis.
- Disturbances in blood flow, inflammation, and smooth muscle cell activation affect connexin expression and gap junction communication.
- Genetically modified connexin expression influences the progression of these vascular diseases in mice.
Conclusions:
- Gap junction-mediated intercellular communication plays a significant role in vascular remodeling, atherosclerosis, and restenosis.
- Connexin expression and function are dynamically regulated by various factors in vascular disease.
- Connexin-based strategies may offer future therapeutic potential for treating atherosclerosis and restenosis.
Abstract:
Remodeling of the vascular wall plays a central role in many physiological processes, but also in the pathogenesis of cardiovascular diseases such as atherosclerosis and restenosis. Atherosclerosis represents the major cause of death and disability in adult populations of Western societies. Angioplasty is a common and effective method of treatment for coronary atherosclerosis, but restenosis after the procedure continues to be a serious clinical complication. The development of atherosclerosis and restenosis involves complex patterns of interactions between the dysfunctional endothelium, inflammatory cells and smooth muscle cells in which cytokines and growth factors are known to play a critical role. Apart from paracrine cell-to-cell signaling, a role for gap-junction-mediated intercellular communication has recently been suggested. In this chapter, we summarize existing evidence supporting such a role. Thus, the pattern of vascular connexins is altered during atherosclerotic plaque formation and in restenosis. In addition, disturbances in flow, inflammation and smooth muscle cell activation and proliferation have been shown to affect connexin expression or gap junctional communication. Finally, genetically modified connexin expression alters the course of these diseases in mice. Further studies will tell us whether future treatment of atherosclerosis or restenosis may involve connexin-based strategies.
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