Evidence map›Paper›PMID 39505939›Full record

ArticleScientific reports2024

Chemokine receptor CXCR7 antagonism ameliorates cardiac and renal fibrosis induced by mineralocorticoid excess.

Bing H Wang, Remy Robert, Francine Z Marques, Niwanthi Rajapakse, Helen Kiriazis, Charles R Mackay, David M Kaye

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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

7 authors.

Bing H Wang *Heart Failure Research Group, Baker Heart and Diabetes Institute, St Kilda Rd Central, PO Box 6492, Melbourne, VIC, 8008, Australia.
Remy Robert *Department of Physiology, Biodiscovery Research Institute, Faculty of Medicine, Nursing and Health Services, Monash University, Clayton, VIC, Australia.
Francine Z MarquesHeart Failure Research Group, Baker Heart and Diabetes Institute, St Kilda Rd Central, PO Box 6492, Melbourne, VIC, 8008, Australia.
Niwanthi RajapakseHeart Failure Research Group, Baker Heart and Diabetes Institute, St Kilda Rd Central, PO Box 6492, Melbourne, VIC, 8008, Australia.
Helen KiriazisPreclinical Cardiology, Microsurgery, and Imaging Platform, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Charles R MackayDepartment of Physiology, Biodiscovery Research Institute, Faculty of Medicine, Nursing and Health Services, Monash University, Clayton, VIC, Australia. c.mackay@me.com.
David M KayeHeart Failure Research Group, Baker Heart and Diabetes Institute, St Kilda Rd Central, PO Box 6492, Melbourne, VIC, 8008, Australia. david.kaye@baker.edu.au.

Funding

National Health and Medical Research Council 1136080
6 · The paper itself

Abstract

Cardiorenal fibrosis is a common feature of chronic cardiovascular disease and recent data suggests that cytokines and chemokines may also drive fibrosis. Here we tested the hypothesis that CXCR7, a highly conserved chemokine receptor, contributes to cardiac and renal fibrosis. We generated an anti-mouse CXCR7-specific monoclonal antibody (CXCR7 mAb) and tested its anti-fibrotic actions in cardiorenal fibrosis induced using the deoxycorticosterone acetate/uni-nephrectomy (DOCA-UNX) model. CXCR7 mAb treatment (10 mg/kg, twice weekly for 6 weeks) significantly attenuated the development of cardiac and renal fibrosis, and reduced fibrotic and inflammatory gene expression levels, in the absence of an effect on blood pressure. Immunohistochemical analysis demonstrated an increase in the vascular expression of CXCR7 in DOCA-UNX-treated mice. This study demonstrated that a CXCR7 mediated pathway plays a significant role in cardiac and renal fibrosis induced by DOCA-UNX treatment. Accordingly, antagonism of CXCR7 may provide a therapeutic opportunity to mitigate against fibrosis in the setting of mineralocorticoid excess.

Indexed as

FibrosisKidneyReceptors, CXCRAnimalsAntibodies, MonoclonalDisease Models, AnimalKidney DiseasesMaleMiceMice, Inbred C57BLMyocardiumAntibodies, MonoclonalCmkor1 protein, mouseReceptors, CXCRChemokine receptorsCXCR7 antagonistFibrosisMineralocorticoid excess

Identifiers

PMID39505939
PMCPMC11541864

What OpenQuestion holds

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Registered trials

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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.