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The role of the prolactin/vasoinhibin axis in rheumatoid arthritis: an integrative overview
Open accessAbstract
Rheumatoid arthritis (RA) is a chronic, autoimmune, inflammatory disease destroying articular cartilage and bone. The female preponderance and the influence of reproductive states in RA have long linked this disease to sexually dimorphic, reproductive hormones such as prolactin (PRL). PRL has immune-enhancing properties and increases in the circulation of some patients with RA. However, PRL also suppresses the immune system, stimulates the formation and survival of joint tissues, acquires antiangiogenic properties upon its cleavage to vasoinhibins, and protects against joint destruction and inflammation in the adjuvant-induced model of RA. This review addresses risk factors for RA linked to PRL, the effects of PRL and vasoinhibins on joint tissues, blood vessels, and immune cells, and the clinical and experimental data associating PRL with RA. This information provides important insights into the pathophysiology of RA and highlights protective actions of the PRL/vasoinhibin axis that could lead to therapeutic benefits.
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“Other inflammation-related genes dysregulated in hEDS/HSD include SPON2, up-regulated in patients’ cells, which encodes an ECM protein with multifunctional properties in the innate immune system and inflammatory cell recruitment [152,153,154], and PRLR, showing a decreased expression in hEDS/HSD cells, which encode the prolactin receptor implicated in inflammatory responses and immune cells”
From Cellular and Molecular Mechanisms in the Pathogenesis of Classical, Vascular, and Hypermobile Ehlers‒Danlos Syndromes (2019) · cites this paper as [155]
In the citing paper
“Other inflammation-related genes dysregulated in hEDS/HSD include SPON2, up-regulated in patients’ cells, which encodes an ECM protein with multifunctional properties in the innate immune system and inflammatory cell recruitment [152,153,154], and PRLR, showing a decreased expression in hEDS/HSD cells, which encode the prolactin receptor implicated in inflammatory responses and immune cells”
From Cellular and Molecular Mechanisms in the Pathogenesis of Classical, Vascular, and Hypermobile Ehlers‒Danlos Syndromes (2019) · cites this paper as [155]
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Metadata
- Authors
- Clapp, C., Adán, N., Ledesma-Colunga, M. G., Solís-Gutiérrez, M., Triebel, J., & Martínez de la Escalera, G.
- Affiliations
- Universidad Nacional Autónoma de México (MX)
- Paracelsus Medizinische Privatuniversität (DE)
- Corresponding author
- Clapp, Carmen
- Venue
- Cellular and Molecular Life Sciences
- Published
- 2016-03-29
- Volume
- 73
- Issue
- 15
- Pages
- 2929-2948
- ISSN
- 1420-682X (ISSN-L)
- 1420-9071
- PMC
- PMC11108309
- OpenAlex
- W2321665593
- Cited by
- 38
- References
- 272
- Citations by year
- 2026: 5 · 2025: 2 · 2024: 6 · 2023: 2 · 2022: 4 · 2021: 4 · 2020: 2 · 2019: 8 · 2018: 1 · 2017: 3 · 2016: 1
- FWCI
- 0.68
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cellular and Molecular Life Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Dirección General Asuntos del Personal Académico, Universidad Nacional Autónoma de México (MX) (IN201315)
- Topics
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Health Sciences › Medicine › Complementary and alternative medicine › Natural Compounds in Disease Treatment
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Keywords
- rheumatoid arthritis, prolactin, vasoinhibin, sex differences, reproductive hormones, immune regulation, antiangiogenic activity, joint destruction, risk factors, therapeutic target
- MeSH terms
- Animals, Arthritis, Rheumatoid, Cartilage, Articular, Female, Humans, Immune Tolerance, Immunity, Cellular, Inflammation, Joints, Male, Prolactin, Reproduction, Sex Factors, Stress, Physiological, Stress, Psychological, Angiogenesis Inhibitors
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 ›
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