ArticleJournal of the American Heart Association2014
Anti-remodeling and anti-fibrotic effects of the neuregulin-1β glial growth factor 2 in a large animal model of heart failure.
Article in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 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.
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Who cites it
48 citing papers in PubMed, 83 citations in OpenAlex.
- Species-specific effects of neuregulin-1β (cimaglermin alfa) on glucose handling in animal models and humans with heart failure.Toxicology and applied pharmacology · 2017Trial
- Radiotherapy-Induced Side Effects: Epidemiology, Pathogenesis, Prevention and Treatments.MedComm · 2026Review
- Coronary Microvascular Dysfunction: Epidemiology, Pathophysiology, Diagnosis, and Treatment.MedComm · 2026Review
- Avenues for optimization of cardiac therapeutics by minimally invasive delivery.Acta biomaterialia · 2026Review
- Location and aetiology are determinants of fibroblast activation and heterogeneity in the failing human heart.Genome medicine · 2025Article
- Systems analysis reveals neuregulin-1 control of cardiomyocyte size and shape mediated by distinct PI3K and p38 pathways.bioRxiv : the preprint server for biology · 2025Article
- Nanoscale piezoelectric patches preserve electrical integrity of infarcted hearts.Materials today. Bio · 2025Article
- Geroscience in heart failure: the search for therapeutic targets in the shared pathobiology of human aging and heart failure.The journal of cardiovascular aging · 2025Article
- ALKBH5 induces fibroblast-to-myofibroblast transformation during hypoxia to protect against cardiac rupture after myocardial infarction.Journal of advanced research · 2024Article
- Lupus dermal fibroblasts are proinflammatory and exhibit a profibrotic phenotype in scarring skin disease.JCI insight · 2024Article
- The case for neuregulin-1 as a clinical treatment for stroke.Frontiers in cellular neuroscience · 2024Review
- Emerging Therapy for Diabetic Cardiomyopathy: From Molecular Mechanism to Clinical Practice.Biomedicines · 2023Review
- Reproducing extracellular matrix adverse remodelling of non-ST myocardial infarction in a large animal model.Nature communications · 2023Article
- Cardiac inducing colonies halt fibroblast activation and induce cardiac/endothelial cells to move and expand via paracrine signaling.Molecular biology of the cell · 2022Article
- From Classic to Modern Prognostic Biomarkers in Patients with Acute Myocardial Infarction.International journal of molecular sciences · 2022Review
- Neuregulin (NRG-1β) Is Pro-Myogenic and Anti-Cachectic in Respiratory Muscles of Post-Myocardial Infarcted Swine.Biology · 2022Article
- Advances and Challenges in Biomarkers Use for Coronary Microvascular Dysfunction: From Bench to Clinical Practice.Journal of clinical medicine · 2022Review
- The Potential of Gamma Secretase as a Therapeutic Target for Cardiac Diseases.Journal of personalized medicine · 2021Review
- Pathomechanisms and therapeutic opportunities in radiation-induced heart disease: from bench to bedside.Clinical research in cardiology : official journal of the German Cardiac Society · 2021Review
- Neuregulins: protective and reparative growth factors in multiple forms of cardiovascular disease.Clinical science (London, England : 1979) · 2020Review
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
20 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundNeuregulin-1β (NRG-1β) is a growth factor critical for cardiac development and repair with therapeutic potential for heart failure. We previously showed that the glial growth factor 2 (GGF2) isoform of NRG-1β improves cardiac function in rodents after myocardial infarction (MI), but its efficacy in a large animal model of cardiac injury has not been examined. We therefore sought to examine the effects of GGF2 on ventricular remodeling, cardiac function, and global transcription in post-MI swine, as well as potential mechanisms for anti-remodeling effects. METHODS AND
resultsMI was induced in anesthetized swine (n=23) by intracoronary balloon occlusion. At 1 week post-MI, survivors (n=13) received GGF2 treatment (intravenous, biweekly for 4 weeks; n=8) or were untreated (n=5). At 5 weeks post-MI, fractional shortening was higher (32.8% versus 25.3%, P=0.019), and left ventricular (LV) end-diastolic dimension lower (4.5 versus 5.3 cm, P=0.003) in GGF2-treated animals. Treatment altered expression of 528 genes, as measured by microarrays, including collagens, basal lamina components, and matricellular proteins. GGF2-treated pigs exhibited improvements in LV cardiomyocyte mitochondria and intercalated disk structures and showed less fibrosis, altered matrix structure, and fewer myofibroblasts (myoFbs), based on trichrome staining, electron microscopy, and immunostaining. In vitro experiments with isolated murine and rat cardiac fibroblasts demonstrate that NRG-1β reduces myoFbs, and suppresses TGFβ-induced phospho-SMAD3 as well as αSMA expression.
conclusionsThese results suggest that GGF2/NRG-1β prevents adverse remodeling after injury in part via anti-fibrotic effects in the heart.
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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.