ArticleNature medicine2011
GDF-15 is an inhibitor of leukocyte integrin activation required for survival after myocardial infarction in mice.
Article in Nature medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04437628 (Prognostic Value Of Short-Term Follow-up Biomarkers After Discharge In hOspitalized Patients With Acute Heart Failure), which is not on this map. Cited by 279 papers, 2 of them syntheses 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.
Prognostic Value Of Short-Term Follow-up Biomarkers After Discharge In hOspitalized Patients With Acute Heart Failure
Who cites it
279 citing papers in PubMed, 2 syntheses or guidelines pooled it, 508 citations in OpenAlex.
- A systematic review of the neuroprotective role and biomarker potential of GDF15 in neurodegeneration.Frontiers in immunology · 2024Pooled it
- Immunomodulatory interventions in myocardial infarction and heart failure: a systematic review of clinical trials and meta-analysis of IL-1 inhibition.Cardiovascular research · 2018Pooled it
- Association of Cardiac Biomarkers in Combination With Cognitive Impairment After Acute Ischemic Stroke.Journal of the American Heart Association · 2024Trial
- GDF15 in Liver Fibrosis: Molecular Mechanisms, Immunoregulatory Functions, and Therapeutic Potential.Biomolecules · 2026Review
- Gdf15 expression in thermogenic adipocytes regulates diet-induced weight gain in a sex-dependent manner.Molecular medicine (Cambridge, Mass.) · 2026Article
- GFRAL is required to mediate changes in systemic metabolism in response to mitochondrial stress in brown adipose tissue.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Local to Systemic Inflammation-From Generation to Prognosis in Acute Coronary Syndrome.Biomedicines · 2026Review
- The Role of GDF-15 in Heart Failure and Biomarker Potential-From Basic Science to Clinical Praxis.Biology · 2026Review
- Pregnancy quenches inflammation through neuroimmune crosstalk.Nature immunology · 2026Article
- A GDF-15-GFRAL axis controls autoimmune T cell responses during neuroinflammation.Nature immunology · 2026Article
- GDF15 induces excessive activation of osteoclasts within the vertebral endplates leading to early endplate degeneration.JCI insight · 2026Article
- GDF15 as a sentinel of metabolic integrity: a narrative review of stress signaling, multisystem pathophysiology, and therapeutic potential.Frontiers in endocrinology · 2026Review
- Plasma protein GDF15 has a good predictive potential for the kidney complications of type 2 diabetes.Frontiers in endocrinology · 2026Article
- Growth differentiation factor 15 (GDF-15) as an emerging biomarker for cardiovascular and kidney diseases, a therapeutic target in cancer and a potential biomarker for preeclampsia.Frontiers in pharmacology · 2026Article
- Novel Roles of GDF15 in Alleviating Renal Fibrosis: Promoting Autophagy and Lysosome Biogenesis via Inhibition of the PI3K/Akt/mTOR Pathway.Journal of cellular and molecular medicine · 2026Article
- Peritumoral colonic epithelial cell-derived GDF15 sustains colorectal cancer via regulation of glycolysis and histone lactylation.Nature aging · 2025Article
- Prognostic utility of mid-regional pro-adrenomedullin and growth differentiation factor 15 in patients undergoing transfemoral transcatheter aortic valve implantation.Clinical research in cardiology : official journal of the German Cardiac Society · 2025Observational
- GDF15: An emerging disease target and biomarker of metabolic diseases.Journal of endocrinological investigation · 2025Review
- Proteome atlas for mechanistic discovery and risk prediction of diabetic retinopathy.Nature communications · 2025Article
- Cardiac adaptation to endurance exercise training requires suppression of GDF15 via PGC-1α.Nature cardiovascular research · 2025Article
219 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory cell recruitment after myocardial infarction needs to be tightly controlled to permit infarct healing while avoiding fatal complications such as cardiac rupture. Growth differentiation factor-15 (GDF-15), a transforming growth factor-β (TGF-β)-related cytokine, is induced in the infarcted heart of mice and humans. We show that coronary artery ligation in Gdf15-deficient mice led to enhanced recruitment of polymorphonuclear leukocytes (PMNs) into the infarcted myocardium and an increased incidence of cardiac rupture. Conversely, infusion of recombinant GDF-15 repressed PMN recruitment after myocardial infarction. In vitro, GDF-15 inhibited PMN adhesion, arrest under flow and transendothelial migration. Mechanistically, GDF-15 counteracted chemokine-triggered conformational activation and clustering of β(2) integrins on PMNs by activating the small GTPase Cdc42 and inhibiting activation of the small GTPase Rap1. Intravital microscopy in vivo in Gdf15-deficient mice showed that Gdf-15 is required to prevent excessive chemokine-activated leukocyte arrest on the endothelium. Genetic ablation of β(2) integrins in myeloid cells rescued the mortality of Gdf15-deficient mice after myocardial infarction. To our knowledge, GDF-15 is the first cytokine identified as an inhibitor of PMN recruitment by direct interference with chemokine signaling and integrin activation. Loss of this anti-inflammatory mechanism leads to fatal cardiac rupture after myocardial infarction.
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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.