Lupus & antiphospholipid syndrome
Elevated integrin αvβ3 expression activates the NF-κB p65/p100 pathway and promotes inflammatory responses in systemic lupus erythematosus
Authors' conclusion
This study highlights that the upregulation of integrin αvβ3 expression in SLE activates the NF-κB p65/p100 pathway, which plays a pivotal role in orchestrating inflammatory responses.
Study context
- Population
- Patients with systemic lupus erythematosus (SLE), healthy controls and MRL/lpr lupus mice
- Participants
- 36 vs 36
- Comparison
- Patients with SLE vs healthy controls; integrin αvβ3 antagonist SB273005 in MRL/lpr lupus mice
- SLEn = 36
- Healthy controln = 36reference
Methodological detailsin vivo and in vitro, MRL/lpr lupus mouse model, Western blot and immunohistochemistry staining, Student's t-test, ANOVA and post-hoc Kruskal-Wallis tests
- In vivo and in vitro
- MRL/lpr lupus mouse model
- Western blot and immunohistochemistry staining
- Student's t-test, ANOVA and post-hoc Kruskal-Wallis tests
Main finding
As reported in the abstract
- Elevated integrin αvβ3 expression in serum, skin and renal tissues of patients with SLE, contributing to NF-κB activation
- Enhanced synthesis of NF-κB p65 and p100, promoting NF-κB activation and dysregulation of TLR7 expression
- Increase in inflammatory factors such as TNF-α and IL-6, making skin and kidneys more susceptible to inflammation
- SB273005 in MRL/lpr mice significantly reduced NF-κB p65/p100 synthesis, suppressed NF-κB activation, decreased inflammatory factors in serum and kidneys and alleviated organ damage
Original publication
Elevated integrin αvβ3 expression activates the NF-κB p65/p100 pathway and promotes inflammatory responses in systemic lupus erythematosus. Clin Exp Rheumatol. Published 26 January 2025. doi:10. 55563/ clinexprheumatol/ 0cfcsp
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