ArticleInflammation2025
Low-Protein Diet Inhibits the Synovial Tissue Macrophage Pro-Inflammatory Polarization Via NRF2/SIRT3/SOD2/ROS Pathway in K/BxN Rheumatoid Arthritis Mice.
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Engineered probiotics constitutively expressing SOD alleviate inflammatory bowel disease by targeting ROS.iScience · 2026Article
- SIRT3 deficiency impairs mitochondrial bioenergetics via hyperacetylation of TCA cycle enzymes in chronic heart failure.Journal of translational medicine · 2026Article
- Metabolic-epigenetic rewiring in rheumatoid arthritis: from pathogenic memory to precision restoration.Frontiers in immunology · 2026Review
- The Nrf2/HO-1 signaling pathway in arthritis: from molecular mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- Nrf2 as a redox checkpoint in autoimmune joint inflammation: microenvironmental redox control across the arthritis spectrum.Frontiers in immunology · 2026Review
- Integrating Nutrition into Precision Medicine for Controlling Systemic Inflammation in Rheumatoid Arthritis.Inflammation · 2025Review
- Mitochondrial metabolic regulation of macrophage polarization in osteomyelitis and other orthopedic disorders: mechanisms and therapeutic opportunities.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized by pain, swelling, stiffness, and impaired function. Attenuating inflammation is a crucial objective in RA management. Diet and nutrition are believed to influence RA symptomatology, with a low-protein diet being one potential nutritional strategy, although its underlying mechanisms remain to be fully elucidated. In this research, serum derived from arthritic transgenic K/BxN mice was administered to naive mice to establish a K/BxN rheumatoid arthritis model. Physiological assessments and histological staining were performed to evaluate joint pathology. (Enzyme-linked immunosorbent assay) ELISA was used to measure inflammatory cytokines. Flow cytometry and immunofluorescence were applied to characterize macrophage phenotypes. Transcriptomic analysis elucidated molecular pathways under the effect of a low-protein diet and verified by immunoblotting. Mitochondrial reactive oxygen species (ROS) was detected by Mito-SOX. Protein expression was silenced through the application of siRNA transfection. Our results indicate that a low-protein diet significantly alleviates disease symptoms and decreases pro-inflammatory cytokine levels in synovial fluid. Furthermore, this dietary intervention inhibits M1 macrophage polarization while promoting a shift towards the M2 phenotype. Transcriptomic analysis revealed that the beneficial effects of the low-protein diet in alleviating rheumatoid arthritis are closely linked to the NRF2 pathway. In vitro, low protein treatment can promote the activity of NRF2 via inhibiting the ubiquitin mediated proteolysis and activate the NRF2/SIRT3/SOD2 pathway to inhibit the production of ROS, which will further inhibit the M1 macrophage polarization. NRF2 knockdown can abolish the effects of low-protein treatment, indicating that the inhibition of M1 polarization and the anti-inflammatory response induced by low-protein treatment are dependent on NRF2. In summary, our findings propose that low-protein diet can inhibit synovial macrophage M1 polarization via activating NRF2/SIRT3/SOD2 pathway to reduce mitochondrial ROS production. This mechanism effectively decreases synovial inflammation and alleviates RA symptoms.
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Registered trials
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