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Published on: October 17, 2017
Chronic inflammation and vascular cell plasticity in atherosclerosis
Alexander Lin1,2, Joseph M Miano3, Edward A Fisher4,5
1Atherosclerosis and Vascular Remodelling Group, Heart Research Institute, Sydney, New South Wales, Australia.
Insights
Vascular cells change phenotypes during atherosclerosis, influencing plaque inflammation and stability. Targeting these cell phenotype changes offers a novel therapeutic strategy for cardiovascular disease.
Area of Science:
- Cardiovascular Research
- Cell Biology
- Immunology
Background:
- Atherosclerosis involves dynamic changes in vascular cells (smooth muscle cells, endothelial cells, macrophages) driven by chronic inflammation.
- The inflammatory hypothesis of atherosclerosis is supported by clinical trials showing anti-inflammatory therapy reduces cardiovascular events.
- Current therapies do not specifically target the diverse phenotypes of cells within atherosclerotic plaques.
Purpose of the Study:
- To review vascular cell plasticity within the atherosclerotic plaque microenvironment.
- To emphasize the link between vascular cell phenotype, plaque inflammation, and lesion stability.
- To propose modulating plaque cell phenotype as a new therapeutic approach for atherosclerosis.
Main Methods:
- Review of existing literature on vascular cell plasticity in atherosclerosis.
- Analysis of evidence linking cell phenotype to plaque inflammation and stability.
- Discussion of therapeutic implications of targeting cell phenotypes.
Main Results:
- Vascular cell phenotypic conversions are integral to atherosclerosis progression and inflammation.
- Cellular plasticity within plaques is closely tied to inflammation and lesion stability.
- Understanding cell behavior during therapy is crucial for effective treatment.
Conclusions:
- Vascular cell plasticity is a key factor in atherosclerosis, influenced by the inflammatory microenvironment.
- Targeting the phenotype of plaque cells presents an unexplored therapeutic avenue.
- Further research is needed to understand and manipulate cell phenotypes for atherosclerosis treatment.
Abstract:
Vascular smooth muscle cells, endothelial cells and macrophages undergo phenotypic conversions throughout atherosclerosis progression, both as a consequence of chronic inflammation and as subsequent drivers of it. The inflammatory hypothesis of atherosclerosis has been catapulted to the forefront of cardiovascular research as clinical trials have shown that anti-inflammatory therapy reduces adverse cardiovascular events. However, no current therapies have been specifically designed to target the phenotype of plaque cells. Fate mapping has revealed that plaque cells convert to detrimental and beneficial cell phenotypes during atherosclerosis, with cumulative evidence highlighting that vascular cell plasticity is intimately linked with plaque inflammation, ultimately impacting lesion stability. Here we review vascular cell plasticity during atherosclerosis in the context of the chronic inflammatory plaque microenvironment. We highlight the need to better understand how plaque cells behave during therapeutic intervention. We then propose modulating plaque cell phenotype as an unexplored therapeutic paradigm in the clinical setting.
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