Evidence map›Paper›PMID 42804830›Full record

ArticleJACC. Basic to translational science2026

The CXCL12γ/ACKR3 Axis Is a Critical Determinant of Myocardial Angiogenesis and Functional Recovery After Infarction.

Vincent Duval, Morgane Aubert, Alina Ramazanova, Paul Alayrac, Ecem T Sakalli, Clément Cochain, Feriel Hamidou, Alexandra Achab Ali, Jose Vilar, Mathilde Lemitre and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JACC. Basic to translational science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

17 authors.

Vincent DuvalUniversité Paris Cité, PARCC, INSERM, Paris, France.
Morgane AubertUniversité Paris Cité, PARCC, INSERM, Paris, France.
Alina RamazanovaUniversité Paris Cité, PARCC, INSERM, Paris, France.
Paul AlayracUniversité Paris Cité, PARCC, INSERM, Paris, France.
Ecem T SakalliInstitute of Experimental Biomedicine, University Hospital Würzburg, Würzburg, Germany; Comprehensive Heart Failure Center Würzburg, University Hospital Würzburg, Würzburg, Germany.
Clément CochainUniversité Paris Cité, PARCC, INSERM, Paris, France; Institute of Experimental Biomedicine, University Hospital Würzburg, Würzburg, Germany; Comprehensive Heart Failure Center Würzburg, University Hospital Würzburg, Würzburg, Germany.
Feriel HamidouUniversité Paris Cité, PARCC, INSERM, Paris, France.
Alexandra Achab AliUniversité Paris Cité, PARCC, INSERM, Paris, France.
Jose VilarUniversité Paris Cité, PARCC, INSERM, Paris, France.
Mathilde LemitreUniversité Paris Cité, PARCC, INSERM, Paris, France.
Stéphane M CamusUniversité Paris Cité, PARCC, INSERM, Paris, France.
Bernard MasriUniversité Paris Cité, CNRS, Inserm, Institut Cochin, Paris, France.
Ralf JockersUniversité Paris Cité, CNRS, Inserm, Institut Cochin, Paris, France.
Julie DamUniversité Paris Cité, CNRS, Inserm, Institut Cochin, Paris, France.
Thierry DurrouxIGF, Université de Montpellier, CNRS, INSERM, Montpellier, France.
Jean-Sébastien SilvestreUniversité Paris Cité, PARCC, INSERM, Paris, France. Electronic address: jean-sebastien.silvestre@inserm.fr.
Angélique LevoyeUniversité Paris Cité, PARCC, INSERM, Paris, France; Université Sorbonne Paris Nord, Bobigny, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Following myocardial infarction, the CXCL12γ-heparan sulfate-ACKR3 axis emerges as a critical, localized signaling mechanism for cardiac repair. Unlike the α isoform, CXCL12γ exhibits superior affinity for ACKR3. Although genetic disruption of CXCL12γ-heparan sulfate binding impairs postischemic angiogenesis and function, its overexpression rescues these deficits. Mechanistically, cardiomyocyte-specific ACKR3 is vital for the regulation of cardiac function, whereas fibroblast-specific ACKR3 orchestrates a proangiogenic paracrine program. This study identifies CXCL12γ as a noncanonical ligand that activates fibroblast-mediated microvascular expansion via ACKR3, offering a novel therapeutic target to enhance myocardial recovery and preserve cardiac performance.

Indexed as

angiogenesischemokinesextracellular matrixfibroblastsmyocardial infarction

Identifiers

PMID42804830
PMCPMC13521161

What OpenQuestion holds

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Read underepoch 390

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.