Molecular and cellular mechanisms of inflammation in atherosclerosis.
| Autor: | Popa-Fotea NM; Department 4 Cardio-Thoracic Pathology, University of Medicine and Pharmacy 'Carol Davila,' Bucharest, Romania.; Cardiology Department, Emergency Clinical Hospital, Bucharest, Romania., Ferdoschi CE; Department 4 Cardio-Thoracic Pathology, University of Medicine and Pharmacy 'Carol Davila,' Bucharest, Romania., Micheu MM; Cardiology Department, Emergency Clinical Hospital, Bucharest, Romania. |
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| Jazyk: | angličtina |
| Zdroj: | Frontiers in cardiovascular medicine [Front Cardiovasc Med] 2023 Aug 03; Vol. 10, pp. 1200341. Date of Electronic Publication: 2023 Aug 03 (Print Publication: 2023). |
| DOI: | 10.3389/fcvm.2023.1200341 |
| Abstrakt: | Atherosclerosis and its complications are a major cause of morbidity and mortality worldwide in spite of the improved medical and invasive treatment in terms of revascularization. Atherosclerosis is a dynamic, multi-step process in which inflammation is a ubiquitous component participating in the initiation, development, and entanglements of the atherosclerotic plaque. After activation, the immune system, either native or acquired, is part of the atherosclerotic dynamics enhancing the pro-atherogenic function of immune or non-immune cells, such as endothelial cells, smooth muscle cells, or platelets, through mediators such as cytokines or directly by cell-to-cell interaction. Cytokines are molecules secreted by the activated cells mentioned above that mediate the inflammatory component of atherosclerosis whose function is to stimulate the immune cells and the production of further cytokines. This review provides insights of the cell axis activation and specific mechanisms and pathways through which inflammation actuates atherosclerosis. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (© 2023 Popa-Fotea, Ferdoschi and Micheu.) |
| Databáze: | MEDLINE |
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