ArticleNature cardiovascular research2025
Heart failure-specific cardiac fibroblasts contribute to cardiac dysfunction via the MYC-CXCL1-CXCR2 axis.
Article in Nature cardiovascular research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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.
Who cites it
8 citing papers in PubMed.
- TRIM28 SUMOylates IRF3 in astrocytes to drive neutrophils infiltration and ischemic cerebral injury.Cell death and differentiation · 2026Article
- The Role of Inflammation and Immunity in Cardiovascular Disease: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- MYC promotes myocardial fibrosis via METTL1-mediated m7G modification of HILPDA.Biology direct · 2026Article
- Decoding thebioRxiv : the preprint server for biology · 2026Article
- The role of chemokines and their receptors in cardiovascular diseases.Frontiers in immunology · 2026Review
- Targeted therapies in non-small cell lung cancer and their cardiovascular impact: mechanisms, clinical profiles, and strategies of management.Frontiers in pharmacology · 2026Review
- c-Myc: an emerging participant in heart failure.Frontiers in cardiovascular medicine · 2026Review
- MYC-CXCL1-CXCR2 Axis in Heart Failure-Specific Cardiac Fibroblasts: a Potential Novel Therapeutic Target Beyond Cardiomyocytes.Journal of cardiovascular translational research · 2025Article
Corrections and comments
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Authors and funding
21 authors.
Funding
Abstract
Heart failure (HF) is a growing global health issue. While most studies focus on cardiomyocytes, here we highlight the role of cardiac fibroblasts (CFs) in HF. Single-cell RNA sequencing of mouse hearts under pressure overload identified six CF subclusters, with one specific to the HF stage. This HF-specific CF population highly expresses the transcription factor Myc. Deleting Myc in CFs improves cardiac function without reducing fibrosis. MYC directly regulates the expression of the chemokine CXCL1, which is elevated in HF-specific CFs and downregulated in Myc-deficient CFs. The CXCL1 receptor, CXCR2, is expressed in cardiomyocytes, and blocking the CXCL1-CXCR2 axis mitigates HF. CXCL1 impairs contractility in neonatal rat and human iPSC-derived cardiomyocytes. Human CFs from failing hearts also express MYC and CXCL1, unlike those from controls. These findings reveal that HF-specific CFs contribute to HF via the MYC-CXCL1-CXCR2 pathway, offering a promising therapeutic target beyond cardiomyocytes.
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Registered trials
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.