Notch Signaling Regulates Immune Responses in Atherosclerosis
Atherosclerosis is a chronic autoimmune inflammatory disease that can cause coronary artery disease, stroke, peripheral artery disease, depending on which arteries are affected. At the beginning of atherosclerosis plasma lipoproteins accumulate in the sub-endothelial space. In response, monocytes mi...
| Main Authors: | , , , , , |
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| Format: | Journal Article |
| Language: | English |
| Published: |
FRONTIERS MEDIA SA
2019
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| Subjects: | |
| Online Access: | http://hdl.handle.net/20.500.11937/75819 |
| _version_ | 1848763559077478400 |
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| author | Vieceli Dalla Sega, F. Fortini, F. Aquila, G. Campo, G. Vaccarezza, Mauro Rizzo, P. |
| author_facet | Vieceli Dalla Sega, F. Fortini, F. Aquila, G. Campo, G. Vaccarezza, Mauro Rizzo, P. |
| author_sort | Vieceli Dalla Sega, F. |
| building | Curtin Institutional Repository |
| collection | Online Access |
| description | Atherosclerosis is a chronic autoimmune inflammatory disease that can cause coronary artery disease, stroke, peripheral artery disease, depending on which arteries are affected. At the beginning of atherosclerosis plasma lipoproteins accumulate in the sub-endothelial space. In response, monocytes migrate from the circulation through the endothelium into the intima where they differentiate into macrophages. These early events trigger a complex immune response that eventually involves many cellular subtypes of both innate and adaptive immunity. The Notch signaling pathway is an evolutionary conserved cell signaling system that mediates cell-to-cell communication. Recent studies have revealed that Notch modulate atherosclerosis by controlling macrophages polarization into M1 or M2 subtypes. Furthermore, it is known that Notch signaling controls differentiation and activity of T-helper and cytotoxic T-cells in inflammatory diseases. In this review, we will discuss the role of Notch in modulating immunity in the context of atherosclerosis and whether targeting Notch may represent a therapeutic strategy. |
| first_indexed | 2025-11-14T11:05:23Z |
| format | Journal Article |
| id | curtin-20.500.11937-75819 |
| institution | Curtin University Malaysia |
| institution_category | Local University |
| language | English |
| last_indexed | 2025-11-14T11:05:23Z |
| publishDate | 2019 |
| publisher | FRONTIERS MEDIA SA |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | curtin-20.500.11937-758192019-07-11T00:42:09Z Notch Signaling Regulates Immune Responses in Atherosclerosis Vieceli Dalla Sega, F. Fortini, F. Aquila, G. Campo, G. Vaccarezza, Mauro Rizzo, P. Science & Technology Life Sciences & Biomedicine Immunology atherosclerosis endothelial dysfunction Notch DII4 immunity M1 macrophages T cells GSI GAMMA-SECRETASE INHIBITORS IN-VIVO FUNCTION T-CELL FUNCTION DENDRITIC CELLS TH17 CELLS MACROPHAGE POLARIZATION SUPPRESSOR-CELLS RBP-J VASCULAR ENDOTHELIUM GATA3 EXPRESSION Atherosclerosis is a chronic autoimmune inflammatory disease that can cause coronary artery disease, stroke, peripheral artery disease, depending on which arteries are affected. At the beginning of atherosclerosis plasma lipoproteins accumulate in the sub-endothelial space. In response, monocytes migrate from the circulation through the endothelium into the intima where they differentiate into macrophages. These early events trigger a complex immune response that eventually involves many cellular subtypes of both innate and adaptive immunity. The Notch signaling pathway is an evolutionary conserved cell signaling system that mediates cell-to-cell communication. Recent studies have revealed that Notch modulate atherosclerosis by controlling macrophages polarization into M1 or M2 subtypes. Furthermore, it is known that Notch signaling controls differentiation and activity of T-helper and cytotoxic T-cells in inflammatory diseases. In this review, we will discuss the role of Notch in modulating immunity in the context of atherosclerosis and whether targeting Notch may represent a therapeutic strategy. 2019 Journal Article http://hdl.handle.net/20.500.11937/75819 10.3389/fimmu.2019.01130 English http://creativecommons.org/licenses/by/4.0/ FRONTIERS MEDIA SA fulltext |
| spellingShingle | Science & Technology Life Sciences & Biomedicine Immunology atherosclerosis endothelial dysfunction Notch DII4 immunity M1 macrophages T cells GSI GAMMA-SECRETASE INHIBITORS IN-VIVO FUNCTION T-CELL FUNCTION DENDRITIC CELLS TH17 CELLS MACROPHAGE POLARIZATION SUPPRESSOR-CELLS RBP-J VASCULAR ENDOTHELIUM GATA3 EXPRESSION Vieceli Dalla Sega, F. Fortini, F. Aquila, G. Campo, G. Vaccarezza, Mauro Rizzo, P. Notch Signaling Regulates Immune Responses in Atherosclerosis |
| title | Notch Signaling Regulates Immune Responses in Atherosclerosis |
| title_full | Notch Signaling Regulates Immune Responses in Atherosclerosis |
| title_fullStr | Notch Signaling Regulates Immune Responses in Atherosclerosis |
| title_full_unstemmed | Notch Signaling Regulates Immune Responses in Atherosclerosis |
| title_short | Notch Signaling Regulates Immune Responses in Atherosclerosis |
| title_sort | notch signaling regulates immune responses in atherosclerosis |
| topic | Science & Technology Life Sciences & Biomedicine Immunology atherosclerosis endothelial dysfunction Notch DII4 immunity M1 macrophages T cells GSI GAMMA-SECRETASE INHIBITORS IN-VIVO FUNCTION T-CELL FUNCTION DENDRITIC CELLS TH17 CELLS MACROPHAGE POLARIZATION SUPPRESSOR-CELLS RBP-J VASCULAR ENDOTHELIUM GATA3 EXPRESSION |
| url | http://hdl.handle.net/20.500.11937/75819 |