Copyright: ©Author(s) 2026.
World J Transl Med. Sep 28, 2026; 12(3): 122119
Published online Sep 28, 2026. doi: 10.5528/wjtm.122119
Published online Sep 28, 2026. doi: 10.5528/wjtm.122119
Figure 2 Illustration depict the mechanisms of proinflammatory cytokines in bone-muscle axis (rheumatoid arthritis, osteoarthritis, periodontitis and osteosarcopenia).
Created by Biorender.com. A central cytokine hub connects to panels showing synovitis, cartilage destruction, periodontal bone loss, and bone–muscle wasting. Arrows highlight shared osteoimmunological pathways underlying systemic bone fragility, frailty, falls and fracture risk in aging inflammatory conditions. IL-6: Interleukin-6; TNF-α: Tumor necrosis factor-α; SASP: Senescence-associated secretory phenotype; OPG: Osteoprotegerin; RANKL: Receptor activator of NF-κB ligand; NF-κB: Nuclear factor-κB; JAK–STAT: Janus kinase–signal transducer and activator of transcription; BMD: Bone mineral density.
- Citation: Gunasekar A, Jeyaraman N, Chitra SB, Yudakar V, Bharadwaj S, Muthu S, Jeyaraman M. Interleukin-6 and tumor necrosis factor-α in osteoimmunology: Aging, and anticytokine therapies. World J Transl Med 2026; 12(3): 122119
- URL: https://www.wjgnet.com/2220-6132/full/v12/i3/122119.htm
- DOI: https://dx.doi.org/10.5528/wjtm.122119