The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Pathogenesis of osteoarthritis, rheumatoid arthritis, and hemophilic arthropathy: The role of angiogenesis
Open accessAbstract
Introduction: The term ‘chronic inflammatory arthritis’ (IA) can be used to define a group of heterogeneous diseases in which inflammation of the synovium is the common feature while having different pathogenesis and clinical outcomes. This condition can be found in osteoarthritis (OA), rheumatoid arthritis (RA), and hemophilic arthropathy (HA). Aim: The objective is to try to highlight similarities and differences in the three pathological conditions and understand both molecular and physiological mechanisms. Method: We have carried out a systematic review of the available literature following the guidelines Preferred Reporting Items for Systematic Reviews and Meta‐analysis (PRISMA). Results: By comparing the data in the literature on OA, RA, and HA we have shown that the three pathologies differ in initial etiology but they motivate the same molecular pathways. Conclusion: In this review we highlighted the similarities and differences between these diseases, creating ideas for future studies both in vivo and in vitro to develop new therapeutic agents and suggest possible biomarkers to follow the evolution and severity of the disease.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“Systemic inflammation promotes endothelial dysfunction, whereas local hypoxia within inflamed joints drives pathological angiogenesis, thereby sustaining synovitis and structural damage [120,121].”
From Interorgan Communications in Skeletal Pathophysiology: From Molecular Pathways to Multidisciplinary Therapies (2026) · cites this paper as [120]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Systemic inflammation promotes endothelial dysfunction, whereas local hypoxia within inflamed joints drives pathological angiogenesis, thereby sustaining synovitis and structural damage [120,121].”
From Interorgan Communications in Skeletal Pathophysiology: From Molecular Pathways to Multidisciplinary Therapies (2026) · cites this paper as [120]
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Role of proinflammatory cytokines in the pathophysiology of osteoarthritis
Kapoor, M., Martel-Pelletier, J., Lajeunesse, D., Pelletier, J.-P., & Fahmi, H. (2011) · Nature Reviews Rheumatology · doi:10.1038/nrrheum.2010.196 · Cited by 2,778
Flagged first, then by citations
Research works printed but not linked: 26
- 10.1111/ejh.12227 · DOI
- 10.1038/nrrheum.2012.80 · DOI
- 10.1038/nrrheum.2017.115 · DOI
- 10.1080/17474086.2020.1685867 · DOI
- 10.1080/17474086.2016.1234933 · DOI
- 10.1186/s13075‐017‐1229‐9 · DOI
- 10.3389/fphys.2020.00541 · DOI
- 10.1016/j.bone.2012.02.012 · DOI · Paper page
- 10.1038/s41584‐021‐00682‐3 · DOI · Paper page
- 10.1038/nrdp.2018.1 · DOI
- 10.3389/fimmu.2019.00266 · DOI
- 10.3389/fimmu.2021.678757 · DOI
- 10.3390/cells8020121 · DOI
- 10.1111/hae.14343 · DOI
- 10.1016/j.ejphar.2021.174500 · DOI
- 10.1007/s10456‐015‐9477‐2 · DOI
- 10.7150/ijbs.7502 · DOI
- 10.1007/s00018‐022‐04178‐5 · DOI
- 10.1182/blood‐2010‐05‐284653 · DOI
- 10.1002/ajh.24133 · DOI
- 10.15256/joc.2011.1.2 · DOI
- 10.3390/ijms19072012 · DOI
- 10.4274/tjh.2016.0031 · DOI
- 10.1038/nrrheum.2013.44 · DOI
- 10.1182/blood‐2017‐12‐820571 · DOI
- 10.1001/jama.2018.13103 · DOI
Cited by
Sorted by citations
Gan, D., Qin, L., & Xiao, G. (2026) · Research · doi:10.34133/research.1319 · Cited by 1
“In parallel, vascular dysfunction represents a key convergent mechanism: Systemic inflammation promotes endothelial dysfunction, whereas local hypoxia within inflamed joints drives pathological angiogenesis, thereby sustaining synovitis and structural damage [ 120 , 121 ].”
Metadata
- Authors
- Caliogna, L., Berni, M., Torriani, C., Mancuso, M. E., Di Minno, M. N. D., Brancato, A. M., Jannelli, E., Mosconi, M., & Pasta, G.
- Affiliations
- Policlinico San Matteo Fondazione (IT)
- IRCCS Humanitas Research Hospital (IT)
- Department of Translational Medical Sciences Federico II University Napoli Italy
- University of Pavia (IT)
- Corresponding author
- Pasta, Gianluigi
- ORCID
- Venue
- Haemophilia
- Publisher
- Wiley
- Published
- 2024-09-19
- Volume
- 30
- Issue
- 6
- Pages
- 1256-1264
- ISSN
- 1351-8216 (ISSN-L)
- 1365-2516
- PMC
- PMC11659485
- OpenAlex
- W4402619639
- Cited by
- 39
- References
- 1
- Citations by year
- 2026: 26 · 2025: 13
- FWCI
- 12.63
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Haemophilia (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Health Sciences › Medicine › Hematology › Hemophilia Treatment and Research
- Keywords
- osteoarthritis, rheumatoid arthritis, hemophilic arthropathy, angiogenesis, chronic inflammatory arthritis, synovitis, pathogenesis, molecular pathways, biomarkers, therapeutic target
- MeSH terms
- Angiogenesis, Arthritis, Rheumatoid, Hemarthrosis, Hemophilia A, Humans, Neovascularization, Pathologic, Osteoarthritis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review