SPECIFIC ROLE OF IL-1Β IN URIC ACID-RELATED INFLAMMATION : A NARRATIVE REVIEW
| Autor: | Rona Hawa Kamilah, Salni, Ziske Maritska, Fatmawati |
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| Jazyk: | indonéština |
| Rok vydání: | 2024 |
| Předmět: | |
| Zdroj: | Jurnal Kedokteran dan Kesehatan, Vol 11, Iss 2, Pp 174-181 (2024) |
| Druh dokumentu: | article |
| ISSN: | 2406-7431 2614-0411 |
| DOI: | 10.32539/jkk.v11i2.396 |
| Popis: | Inflammatory conditions in hyperuricemia are caused by monosodium urate crystals that induce the release of IL-1β, marking a crucial milestone in the pathogenesis of hyperuricemia. Several studies have linked the relationship between serum uric acid levels and the release of IL-1β. IL-1β plays a key role in the pathogenesis of gout. The IL-1β signaling is currently considered an initiating event that triggers uric acid inflammation and promotes the recruitment of a large number of neutrophils to the inflammatory site. Neutrophil activation caused by crystals results in the inhibition of apoptosis, degranulation, the release of reactive oxygen species (ROS), TNF-α, IL-1β, and PGE2, as well as the formation of extracellular neutrophil tissue, further reinforcing the inflammatory process. Recent research indicates that hyperuricemia patients have significantly higher levels of IL-1β. Other studies suggest that elevated IL-1β levels correlate with a more severe anatomical pathology in the joint tissues of rat ankles, including synovial hyperplasia, cartilage damage, and bone erosion. |
| Databáze: | Directory of Open Access Journals |
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