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The Influence of Adipokines on Radiographic Damage in Inflammatory Rheumatic Diseases
Open accessAbstract
Inflammatory rheumatic diseases (IRDs) are complex immune-mediated diseases that are characterized by chronic inflammation of the joints. Rheumatoid arthritis (RA) and spondyloarthritis (SpA), including axial SpA (ax SpA) and psoriatic arthritis (PsA), are the most common forms of IRD. Both RA and ax SpA are characterized by a chronic course with progressive structural modifications, namely, cartilage damage and bone erosions in RA and osteoproliferative changes with spinal ossifications in ax SpA. The adipose tissue is involved in the pathophysiology of IRDs via the release of several proteins, namely, adipokines. Several adipokines with pro-inflammatory effects have been identified, such as leptin, adiponectin, visfatin and resistin. In this review, we discuss the role that adipokines may play in the structural modifications of the peripheral joints and/or axial skeleton. In RA, the role of leptin in structural damage remains controversial, while adiponectin and its high-molecular-weight isoform are known to have an influence on the development of bone erosions and radiographic progression. Resistin also appears to be a potent detrimental adipokine for the joints in RA. In ax SpA, visfatin seems to be an attractive candidate for radiographic progression, while leptin and adiponectin have negative effects on radiographic progression.
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“Leptin derived from obesity or periarticular fat depots promotes synovial inflammation, cartilage catabolism, and pain, whereas adiponectin exerts context-dependent effects, including associations with radiographic progression and bone erosion in RA [124–126].”
From Interorgan Communications in Skeletal Pathophysiology: From Molecular Pathways to Multidisciplinary Therapies (2026) · cites this paper as [126]
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“Leptin derived from obesity or periarticular fat depots promotes synovial inflammation, cartilage catabolism, and pain, whereas adiponectin exerts context-dependent effects, including associations with radiographic progression and bone erosion in RA [124–126].”
From Interorgan Communications in Skeletal Pathophysiology: From Molecular Pathways to Multidisciplinary Therapies (2026) · cites this paper as [126]
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Metadata
- Authors
- Toussirot, E.
- Affiliations
- INSERM CIC-1431, Centre d’Investigation Clinique Biothérapie, Pôle Recherche, CHU de Besançon, 25000 Besançon, France
- ORCID
- Toussirot, Eric
- Venue
- Biomedicines
- Publisher
- MDPI AG
- Published
- 2023-02-13
- Volume
- 11
- Issue
- 2
- Pages
- 536
- ISSN
- 2227-9059 (ISSN-L)
- PMC
- PMC9953013
- OpenAlex
- W4320497452
- Cited by
- 12
- References
- 106
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 1 · 2023: 3
- FWCI
- 0.53
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Biomedicines (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- CHU de Besancon (API/2013/37)
- Topics
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Rheumatology › Spondyloarthritis Studies and Treatments
- Keywords
- adipokines, inflammatory rheumatic diseases, radiographic damage, rheumatoid arthritis, axial spondyloarthritis, psoriatic arthritis, leptin, adiponectin, visfatin, resistin, bone erosion, structural joint damage, adipose tissue, radiographic progression
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