Evidence map›Paper›PMID 40617584›Full record

ArticleRMD open2025

Molecular insights into the relationship between sustained CRP elevation and endothelial dysfunction in axial spondyloarthritis.

Laura Cuesta-López, Iván Arias-de la Rosa, Jesús Eduardo Martín-Salazar, Antonio Manuel Barranco, Lourdes Ladehesa-Pineda, Miriam Ruiz-Ponce, María Ángeles Puche Larrubia, Carlos Pérez-Sánchez, Pedro Seguí, Rafaela Ortega and 10 more

Abstract read
In one paragraph

Article in RMD open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Article
  2. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors.

Laura Cuesta-LópezUniversity of Cordoba, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia Hospital, Cordoba, Spain.
Iván Arias-de la RosaGastroenterology, General Hospital of Tomelloso, Tomelloso, Spain.ORCID 0000-0002-1145-4935
Jesús Eduardo Martín-SalazarMaimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Reina Sofia Hospital, Cordoba, Spain.
Antonio Manuel BarrancoMaimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Reina Sofia Hospital, Cordoba, Spain.
Lourdes Ladehesa-PinedaReina Sofia Hospital, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Cordoba, Spain.
Miriam Ruiz-PonceMaimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Reina Sofia Hospital, Cordoba, Spain.
María Ángeles Puche LarrubiaUniversity of Cordoba, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia Hospital, Cordoba, Spain.ORCID 0000-0002-1526-0978
Carlos Pérez-SánchezUniversity of Cordoba, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia Hospital, Cordoba, Spain.
Pedro SeguíRadiology, Reina Sofia Hospital, Cordoba, Spain.
Rafaela OrtegaReina Sofia Hospital, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Cordoba, Spain.
Jerusalem CalvoReina Sofia Hospital, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Cordoba, Spain.
María Carmen Ábalos-AguileraReina Sofia Hospital, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Cordoba, Spain.
Desirée Ruiz-VilchezReina Sofia Hospital, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Cordoba, Spain.
Elena Moreno-CañoMaimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Reina Sofia Hospital, Cordoba, Spain.
Pedro Ortiz-BuitragoMaimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Reina Sofia Hospital, Cordoba, Spain.
Chary Lopez-PedreraMaimonides Biomedical Research Institute of Cordoba (IMIBIC), University of Cordoba, Reina Sofia Hospital, Cordoba, Spain.
Alejandro Escudero-ContrerasUniversity of Cordoba, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia Hospital, Cordoba, Spain.
Eduardo CollantesUniversity of Cordoba, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia Hospital, Cordoba, Spain.
Clementina López-MedinaUniversity of Cordoba, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia Hospital, Cordoba, Spain.ORCID 0000-0002-2309-5837
Nuria BarbarrojaUniversity of Cordoba, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia Hospital, Cordoba, Spain barbarrojan@gmail.com.ORCID 0000-0002-0962-6072

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo investigate the impact of sustained C reactive protein (CRP) elevation on cardiovascular (CV) risk factors, particularly endothelial dysfunction and atherosclerosis, in axial spondyloarthritis (axSpA) patients and to explore the underlying molecular mechanisms.

methods245 axSpA patients were enrolled. Carotid intima-media thickness (CIMT) and microvascular endothelial function (post-ischaemic reactive hyperaemia) were measured. Retrospective CRP measurements from the past 5 years classified patients as having sustained high CRP if >50% of readings were elevated. Serum levels of 184 inflammation and CV disease-related proteins were analysed using a proximity extension assay, and in vitro studies were conducted in human umbilical vein endothelial cells.

results40% of axSpA patients had sustained CRP elevation, showing increased metabolic comorbidities, higher prevalence of atherosclerotic plaques and worse microvascular endothelial function compared with those with intermittent CRP elevations. Proteomic analysis identified 10 altered proteins, with interleukin 6 (IL-6) and CUB domain-containing protein 1 (CDCP-1) linked to endothelial dysfunction, higher CIMT and metabolic disturbances. Paraoxonase 3 (PON-3), the only downregulated protein, showed anti-inflammatory, antioxidant and antiatherogenic properties, restoring endothelial function in vitro. CDCP-1 was associated with atherosclerotic plaques and promoted endothelial adhesion, oxidative stress and inflammation in vitro. Anti-TNF-α therapy reduced inflammatory markers, complement components and the atherogenic index, while increasing high density lipoprotein, apolipoprotein A and PON-3 levels and decreasing IL-6 and CDCP-1 levels.

conclusionsSustained CRP elevation in axSpA is strongly linked to increased CV risk, endothelial dysfunction and atherosclerosis. IL-6, CDCP-1 and PON-3 emerge as key mediators connecting inflammation to CV risk. Anti-tumour necrosis factor-α therapy improved the metabolic and inflammatory profile and modulated IL-6, CDCP-1 and PON-3 levels, supporting its role in managing CV risks in axSpA.

Indexed as

Axial SpondyloarthritisC-Reactive ProteinEndothelium, VascularAdultAtherosclerosisBiomarkersCarotid Intima-Media ThicknessFemaleHumansHuman Umbilical Vein Endothelial CellsMaleMiddle AgedProteomicsRetrospective StudiesRisk FactorsBiomarkersC-Reactive ProteinAxial SpondyloarthritisCardiovascular DiseasesInflammationTumor Necrosis Factor Inhibitors

Identifiers

PMID40617584
PMCPMC12228463

What Socratic holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.