Chronic inflammation and vascular cell plasticity in atherosclerosis.
Autor: | Lin A; Atherosclerosis and Vascular Remodelling Group, Heart Research Institute, Sydney, New South Wales, Australia.; School of Biomedical Engineering, Faculty of Engineering, The University of Sydney, Sydney, New South Wales, Australia., Miano JM; Vascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA, USA., Fisher EA; Division of Cardiology, Department of Medicine, New York University Grossman School of Medicine, New York, NY, USA.; Cardiovascular Research Center, New York University Grossman School of Medicine, New York, NY, USA., Misra A; Atherosclerosis and Vascular Remodelling Group, Heart Research Institute, Sydney, New South Wales, Australia. ashish.misra@hri.org.au.; Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia. ashish.misra@hri.org.au. |
---|---|
Jazyk: | angličtina |
Zdroj: | Nature cardiovascular research [Nat Cardiovasc Res] 2024 Dec; Vol. 3 (12), pp. 1408-1423. Date of Electronic Publication: 2024 Dec 09. |
DOI: | 10.1038/s44161-024-00569-y |
Abstrakt: | 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. Competing Interests: Competing interests: The authors declare no competing interests. (© 2024. Springer Nature Limited.) |
Databáze: | MEDLINE |
Externí odkaz: |