ArticleCirculation2019
Wnt5a-Mediated Neutrophil Recruitment Has an Obligatory Role in Pressure Overload-Induced Cardiac Dysfunction.
Article in Circulation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- Myocardial Immune Cells: The Basis of Cardiac Immunology.Journal of immunology (Baltimore, Md. : 1950) · 2023Pooled it
- Coenzyme Q10 mitigates macrophage mediated inflammation in heart following myocardial infarction via the NLRP3/IL1β pathway.BMC cardiovascular disorders · 2024Trial
- Canonical WNT Ligands Produced by Regulatory T Cells Restrain Effector CD4bioRxiv : the preprint server for biology · 2026Article
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- Multifaceted roles of neutrophils in cardiac disease.Journal of leukocyte biology · 2025Review
- Pathophysiological Role of Neutrophil Extracellular Traps in Diet-Induced Obesity and Metabolic Syndrome in Animal Models.Nutrients · 2025Review
- Targeting Wnt Pathways with Small Molecules as New Approach in Cardiovascular Disease.Current cardiology reviews · 2025Review
- Single-cell RNA sequencing reveals that myeloid S100A8/A9 is a novel regulator of the transition from adaptive hypertrophy to heart failure after pressure overload.Theranostics · 2025Article
- Association of Neutrophil Percentage-to-Albumin Ratio with All-Cause and Cardiovascular Mortality in Maintenance Hemodialysis Patients: A Retrospective Study.Journal of inflammation research · 2025Article
- Heart failure, inflammation and exercise.International journal of biological sciences · 2025Review
- Anti-CTLA-4 m2a Antibody Exacerbates Cardiac Injury in Experimental Autoimmune Myocarditis Mice By Promoting Ccl5-Neutrophil Infiltration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The role of NETosis in heart failure.Heart failure reviews · 2024Review
- Myocardial Inflammation in Heart Failure With Reduced and Preserved Ejection Fraction.Circulation research · 2024Review
- Wnt signaling in cardiac development and heart diseases.In vitro cellular & developmental biology. Animal · 2024Review
- Neutrophils are indispensable for adverse cardiac remodeling in heart failure.Journal of molecular and cellular cardiology · 2024Article
- Uncovering hub genes and immunological characteristics for heart failure utilizing RRA, WGCNA and Machine learning.International journal of cardiology. Heart & vasculature · 2024Article
- Disruption of theNature cardiovascular research · 2024Article
- Colchicine Inhibits NETs and Alleviates Cardiac Remodeling after Acute Myocardial Infarction.Cardiovascular drugs and therapy · 2024Article
- The Inflammation-Fibrosis Combined Index: A Novel Marker for Predicting Left Ventricular Reverse Remodeling and Prognosis in Patients with HFrEF.Journal of inflammation research · 2024Article
- Primordial Drivers of Diabetes Heart Disease: Comprehensive Insights into Insulin Resistance.Diabetes & metabolism journal · 2024Review
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 5 countries.
Funding
Abstract
backgroundAlthough the complex roles of macrophages in myocardial injury are widely appreciated, the function of neutrophils in nonischemic cardiac pathology has received relatively little attention.
methodsTo examine the regulation and function of neutrophils in pressure overload-induced cardiac hypertrophy, mice underwent treatment with Ly6G antibody to deplete neutrophils and then were subjected to transverse aortic constriction.
resultsNeutrophil depletion diminished transverse aortic constriction-induced hypertrophy and inflammation and preserved cardiac function. Myeloid deficiency of Wnt5a, a noncanonical Wnt, suppressed neutrophil infiltration to the hearts of transverse aortic constriction-treated mice and produced a phenotype that was similar to the neutropenic conditions. Conversely, mice overexpressing Wnt5a in myeloid cells displayed greater hypertrophic growth, inflammation, and cardiac dysfunction. Neutrophil depletion reversed the Wnt5a overexpression-induced cardiac pathology and eliminated differences in cardiac parameters between wild-type and myeloid-specific Wnt5a transgenic mice.
conclusionsThese findings reveal that Wnt5a-regulated neutrophil infiltration has a critical role in pressure overload-induced heart failure.
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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 OpenQuestion graph.