Cargando…
The role of calmodulin and calmodulin-dependent protein kinases in the pathogenesis of atherosclerosis
Atherosclerosis is a chronic inflammatory disease that triggers severe thrombotic cardiovascular events, such as stroke and myocardial infarction. In atherosclerotic processes, both macrophages and vascular smooth muscle cells (VSMCs) are essential cell components in atheromata formation through pro...
Autor principal: | |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer - Medknow
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9020235/ https://www.ncbi.nlm.nih.gov/pubmed/35465283 http://dx.doi.org/10.4103/tcmj.tcmj_119_21 |
_version_ | 1784689492799520768 |
---|---|
author | Chen, Mei-Fang |
author_facet | Chen, Mei-Fang |
author_sort | Chen, Mei-Fang |
collection | PubMed |
description | Atherosclerosis is a chronic inflammatory disease that triggers severe thrombotic cardiovascular events, such as stroke and myocardial infarction. In atherosclerotic processes, both macrophages and vascular smooth muscle cells (VSMCs) are essential cell components in atheromata formation through proinflammatory cytokine secretion, defective efferocytosis, cell migration, and proliferation, primarily controlled by Ca(2+)-dependent signaling. Calmodulin (CaM), as a versatile Ca(2)+ sensor in diverse cell types, regulates a broad spectrum of Ca(2+)-dependent cell functions through the actions of downstream protein kinases. Thus, this review focuses on discussing how CaM and CaM-dependent kinases (CaMKs) regulate the functions of macrophages and VSMCs in atherosclerotic plaque development based on literature from open databases. A central theme in this review is a summary of the mechanisms and consequences underlying CaMK-mediated macrophage inflammation and apoptosis, which are the key processes in necrotic core formation in atherosclerosis. Another central theme is addressing the role of CaM and CaMK-dependent pathways in phenotypic modulation, migration, and proliferation of VSMCs in atherosclerotic progression. A complete understanding of CaM and CaMK-controlled individual processes involving macrophages and VSMCs in atherogenesis might provide helpful information for developing potential therapeutic targets and strategies. |
format | Online Article Text |
id | pubmed-9020235 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Wolters Kluwer - Medknow |
record_format | MEDLINE/PubMed |
spelling | pubmed-90202352022-04-21 The role of calmodulin and calmodulin-dependent protein kinases in the pathogenesis of atherosclerosis Chen, Mei-Fang Tzu Chi Med J Review Article Atherosclerosis is a chronic inflammatory disease that triggers severe thrombotic cardiovascular events, such as stroke and myocardial infarction. In atherosclerotic processes, both macrophages and vascular smooth muscle cells (VSMCs) are essential cell components in atheromata formation through proinflammatory cytokine secretion, defective efferocytosis, cell migration, and proliferation, primarily controlled by Ca(2+)-dependent signaling. Calmodulin (CaM), as a versatile Ca(2)+ sensor in diverse cell types, regulates a broad spectrum of Ca(2+)-dependent cell functions through the actions of downstream protein kinases. Thus, this review focuses on discussing how CaM and CaM-dependent kinases (CaMKs) regulate the functions of macrophages and VSMCs in atherosclerotic plaque development based on literature from open databases. A central theme in this review is a summary of the mechanisms and consequences underlying CaMK-mediated macrophage inflammation and apoptosis, which are the key processes in necrotic core formation in atherosclerosis. Another central theme is addressing the role of CaM and CaMK-dependent pathways in phenotypic modulation, migration, and proliferation of VSMCs in atherosclerotic progression. A complete understanding of CaM and CaMK-controlled individual processes involving macrophages and VSMCs in atherogenesis might provide helpful information for developing potential therapeutic targets and strategies. Wolters Kluwer - Medknow 2021-10-05 /pmc/articles/PMC9020235/ /pubmed/35465283 http://dx.doi.org/10.4103/tcmj.tcmj_119_21 Text en Copyright: © 2021 Tzu Chi Medical Journal https://creativecommons.org/licenses/by-nc-sa/4.0/This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. |
spellingShingle | Review Article Chen, Mei-Fang The role of calmodulin and calmodulin-dependent protein kinases in the pathogenesis of atherosclerosis |
title | The role of calmodulin and calmodulin-dependent protein kinases in the pathogenesis of atherosclerosis |
title_full | The role of calmodulin and calmodulin-dependent protein kinases in the pathogenesis of atherosclerosis |
title_fullStr | The role of calmodulin and calmodulin-dependent protein kinases in the pathogenesis of atherosclerosis |
title_full_unstemmed | The role of calmodulin and calmodulin-dependent protein kinases in the pathogenesis of atherosclerosis |
title_short | The role of calmodulin and calmodulin-dependent protein kinases in the pathogenesis of atherosclerosis |
title_sort | role of calmodulin and calmodulin-dependent protein kinases in the pathogenesis of atherosclerosis |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9020235/ https://www.ncbi.nlm.nih.gov/pubmed/35465283 http://dx.doi.org/10.4103/tcmj.tcmj_119_21 |
work_keys_str_mv | AT chenmeifang theroleofcalmodulinandcalmodulindependentproteinkinasesinthepathogenesisofatherosclerosis AT chenmeifang roleofcalmodulinandcalmodulindependentproteinkinasesinthepathogenesisofatherosclerosis |