Rôle de l’efferocytose dans l’athérosclérose (notice n° 996860)
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| fixed length control field | 03891cam a2200349 4500500 |
| 005 - DATE AND TIME OF LATEST TRANSACTION | |
| control field | 20250125132850.0 |
| 041 ## - LANGUAGE CODE | |
| Language code of text/sound track or separate title | fre |
| 042 ## - AUTHENTICATION CODE | |
| Authentication code | dc |
| 100 10 - MAIN ENTRY--PERSONAL NAME | |
| Personal name | Rochette, Luc |
| Relator term | author |
| 245 00 - TITLE STATEMENT | |
| Title | Rôle de l’efferocytose dans l’athérosclérose |
| 260 ## - PUBLICATION, DISTRIBUTION, ETC. | |
| Date of publication, distribution, etc. | 2024.<br/> |
| 500 ## - GENERAL NOTE | |
| General note | 69 |
| 520 ## - SUMMARY, ETC. | |
| Summary, etc. | RésuméL’efferocytose est un mécanisme important dans le contrôle des processus inflammatoires. Une efferocytose efficace inhibe l’accumulation de cellules apoptotiques et maintient l’homéostasie avant l’apparition de la nécrose, qui favorise l’inflammation. Pendant l’efferocytose, la fission mitochondriale et le processus du stress oxydatif sont liés à la production d’espèces réactives de l’oxygène et au contrôle du stress oxydatif. L’autophagie joue un rôle important dans l’inhibition de l’inflammation et de l’apoptose, et dans la promotion de l’efferocytose par les cellules inflammatoires activées, en particulier les neutrophiles et les macrophages. L’autophagie impliquant les neutrophiles est activée par la phagocytose des pathogènes ou l’activation de récepteurs spécifiques de reconnaissance. L’autophagie est essentielle pour les principales fonctions des neutrophiles, notamment la dégranulation, le stress oxydatif et la libération des cytokines extracellulaires par ces neutrophiles. L’« échec » de l’efferocytose est un mécanisme clé du développement et de la progression des maladies inflammatoires chroniques, y compris l’athérosclérose, les maladies neurodégénératives et le cancer. L’altération de l’efferocytose dans les macrophages apoptotiques est un facteur déterminant de la gravité de l’athérosclérose et de la vulnérabilité des plaques à leur rupture. La suppression des voies d’efferocytose entraîne une aggravation de l’inflammation et une augmentation de l’athérosclérose. |
| 520 ## - SUMMARY, ETC. | |
| Summary, etc. | Efferocytosis is an important mechanism in the control of inflammatory processes. Efficient efferocytosis inhibits accumulation of apoptotic cells, and maintains homeostasis before the onset of necrosis, which promotes inflammation. During efferocytosis, mitochondrial fission and the oxidative stress process are linked through reactive oxygen species production and oxidative stress control. Autophagy plays an important role in inhibiting inflammation and apoptosis, and in promoting efferocytosis by activated inflammatory cells, particularly neutrophils and macrophages. Autophagy in neutrophils is activated by phagocytosis of pathogens or activation of pattern recognition receptors. Autophagy is essential for major neutrophil functions, including degranulation, oxidative stress and release of neutrophil extracellular cytokines. Failed efferocytosis is a key mechanism driving the development and progression of chronic inflammatory diseases, including atherosclerosis, neurodegenerative diseases and cancer. Impairment of efferocytosis in apoptotic macrophages is a determinant of atherosclerosis severity and the vulnerability of plaques to rupture. Deletion of efferocytosis pathways leads to aggravated inflammation and increased atherosclerosis. |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | efferocytose |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | athérosclérose |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | phagocytose |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | stress oxydatif |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | inflammation |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | efferocytosis |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | oxidative stress |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | phagocytosis |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | atherosclerosis |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | inflammation |
| 700 10 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Rigal, Eve |
| Relator term | author |
| 700 10 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Dogon, Geoffrey |
| Relator term | author |
| 700 10 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Zeller, Marianne |
| Relator term | author |
| 700 10 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Cottin, Yves |
| Relator term | author |
| 700 10 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Vergely, Catherine |
| Relator term | author |
| 786 0# - DATA SOURCE ENTRY | |
| Note | Sang Thrombose Vaisseaux | Volume 36 | 3 | 2024-05-01 | p. 111-116 | 0999-7385 |
| 856 41 - ELECTRONIC LOCATION AND ACCESS | |
| Uniform Resource Identifier | <a href="https://shs.cairn.info/revue-sang-thrombose-vaisseaux-2024-3-page-111?lang=fr&redirect-ssocas=7080">https://shs.cairn.info/revue-sang-thrombose-vaisseaux-2024-3-page-111?lang=fr&redirect-ssocas=7080</a> |
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