ArticleJournal of cell communication and signaling2025
Regulation of phosphatase and tensin homolog by complement component 5a (C5a) and its receptor (C5aR1) in lupus nephritis: A novel therapeutic target.
Article in Journal of cell communication and signaling, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Regulation of phosphatase and tensin homolog by complement component 5a (C5a) and its receptor (C5aR1) in lupus nephritis: A novel therapeutic target.Journal of cell communication and signaling · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lupus nephritis (LN), a renal manifestation of systemic lupus erythematosus, results from immune-mediated kidney injury. The present study investigated how complement component 5a (C5a) and its receptor (C5aR1) regulate phosphatase and tensin homolog (PTEN) expression and the phosphoinositide 3-kinase (PI3K)/AKT pathway during LN development. Using MRL/lpr mice as an LN model, we examined the expression of C5a, C5aR1, PTEN, and related proteins through Western blot, quantitative real-time PCR, and immunohistochemistry. Treatment with a C5aR1 antagonist (C5aR1A) was administered to assess its effects on renal function and molecular parameters. Elevated expression of C5a and C5aR1 was detected in MRL/lpr mice, accompanied by reduced PTEN levels and enhanced PI3K/AKT signaling activity. Treatment with the C5aR1 antagonist (C5aR1A) restored PTEN expression, suppressed AKT phosphorylation, and improved renal function, reflected by lower serum creatinine and blood urea nitrogen concentrations. These findings suggest that the C5a/C5aR1 axis contributes to LN progression by regulating PTEN and the PI3K/AKT signaling pathway, offering potential therapeutic insights for LN treatment.
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