ArticleJournal of molecular histology2026
Angiotensin-(1-7) attenuates collagen-induced arthritis and suppresses ferroptosis in THP-1-derived macrophages: involvement of p53/SLC7A11 signaling.
Article in Journal of molecular histology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Rheumatoid arthritis (RA) is characterized by persistent synovial inflammation and progressive joint destruction, while ferroptosis has emerged as a potential contributor to inflammatory tissue injury. This study investigated whether angiotensin-(1-7) [Ang-(1-7)] attenuates arthritis by regulating ferroptosis and explored the involvement of p53/solute carrier family 7 member 11 (SLC7A11) signaling. Bioinformatic analysis of the GSE55235 dataset was performed to identify ferroptosis-related differentially expressed genes in RA. A collagen-induced arthritis (CIA) mouse model and erastin-treated THP-1-derived macrophages were used to evaluate the effects of Ang-(1-7) in vivo and in vitro. Ferroptosis-related genes in RA were enriched in inflammatory responses, oxidative stress, ferroptosis, and p53 signaling. In CIA mice, Ang-(1-7) reduced paw swelling and arthritis scores, ameliorated synovial inflammation and joint damage, and attenuated iron deposition, lipid peroxidation, and ferroptosis-related molecular alterations. Double-immunofluorescence staining further demonstrated decreased glutathione peroxidase 4 (GPX4) and increased acyl-CoA synthetase long-chain family member 4 (ACSL4) expression in F4/80-positive macrophage areas in CIA joints, both of which were reversed by Ang-(1-7). In erastin-treated THP-1-derived macrophages, Ang-(1-7) improved cell viability, restored glutathione levels, reduced malondialdehyde, reactive oxygen species, lipid reactive oxygen species, and Fe
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