Evidence map›Paper›PMID 27271043›Full record

ArticleJournal of cardiovascular translational research2016

CXCL10 Is a Circulating Inflammatory Marker in Patients with Advanced Heart Failure: a Pilot Study.

Raffaele Altara, Marco Manca, Marleen H Hessel, Yumei Gu, Laura C van Vark, K Martijn Akkerhuis, Jan A Staessen, Harry A J Struijker-Boudier, George W Booz, W Matthijs Blankesteijn

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In one paragraph

Article in Journal of cardiovascular translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% of its field
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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  4. Article
  5. CXCL10 Regulates Pressure Overload-Induced Heart Failure.JACC. Basic to translational science · 2026
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5 more citing papers are in PubMed but not listed here.

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

10 authors at 6 institutions in 4 countries.

Raffaele AltaraDepartment of Pharmacology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands. raltara@umc.edu.
Marco MancaDG-DI, Medical Applications, CERN, Geneva, Switzerland.
Marleen H HesselLeiden University Medical Center, Leiden, The Netherlands.
Yumei GuStudies Coordinating Centre, Research Unit Hypertension, Leuven, Belgium.
Laura C van VarkDepartment of Cardiology, Thoraxcenter, Erasmus MC, Rotterdam, The Netherlands.
K Martijn AkkerhuisDepartment of Cardiology, Thoraxcenter, Erasmus MC, Rotterdam, The Netherlands.
Jan A StaessenStudies Coordinating Centre, Research Unit Hypertension, Leuven, Belgium.
Harry A J Struijker-BoudierDepartment of Pharmacology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.
George W BoozDepartment of Pharmacology and Toxicology, School of Medicine, University of Mississippi Medical Center, 2500 North State St., Jackson, MS, 39216-4505, USA.
W Matthijs BlankesteijnDepartment of Pharmacology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.
Maastricht University · NLErasmus University Rotterdam · NLKU Leuven · BEEuropean Organization for Nuclear Research · CHLeiden University Medical Center · NLUniversity of Mississippi Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemokines are involved in the remodeling of the heart; however, their significance as biomarkers in heart failure is unknown. We observed that circulating CXCR3 receptor chemokines CXCL9 and CXCL10 in a rat model of heart failure were increased 1 week after myocardial infarction. CXCL10 was also increased in both remote and infarcted regions of the heart and remained elevated at 16 weeks; CXCL9 was elevated in the remote area at 1 week. In humans, hierarchical clustering and principal component analysis revealed that circulating CXCL10, MIP-1α, and CD40 ligand were the best indicators for differentiating healthy and heart failure subjects. Serum CXCL10 levels were increased in patients with symptomatic heart failure as indexed by NYHA classification II through IV. The presence of CXCL10, MIP-1α, and CD40 ligand appears to be dominant in patients with advanced heart failure. These findings identify a distinct profile of inflammatory mediators in heart failure patients.

Indexed as

AdultAnimalsBiomarkersCase-Control StudiesCD40 LigandChemokine CCL3Chemokine CXCL10Chemokine CXCL9Cluster AnalysisDisease Models, AnimalFemaleHeart FailureHumansInflammationMaleMiddle AgedBiomarkersCCL3 protein, humanCD40 LigandChemokine CCL3Chemokine CXCL10Chemokine CXCL9CXCL10 protein, humanCxcl10 protein, ratCXCL9 protein, ratCxcr3 protein, ratReceptors, CXCR3ChemokinesCXCR3Immune responseInflammation

Identifiers

PMID27271043
OpenAlexW2410122456

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.