ArticleCell research2017
Cardiotrophin 1 stimulates beneficial myogenic and vascular remodeling of the heart.
Article in Cell research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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.
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Who cites it
25 citing papers in PubMed, 45 citations in OpenAlex.
- Cardiovascular signaling proteins as predictors of the cardiac effects of doxorubicin treatment in children with acute lymphoblastic leukemia.Cardio-oncology (London, England) · 2026Article
- Alternative Polyadenylation Signatures Distinguish Maladaptive Right Ventricular Remodeling in Pulmonary Hypertension: Implications for RNA-Based Diagnostics and Therapeutics.British journal of biomedical science · 2026Article
- 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
- Cardiorenal Syndrome in Right Heart Failure Due to Pulmonary Arterial Hypertension-The Right Ventricle as a Therapeutic Target to Improve Renal Function.Cardiovascular drugs and therapy · 2025Review
- Relationship between CTF1 gene expression and prognosis and tumor immune microenvironment in glioma.European journal of medical research · 2025Article
- Interleukins in Epilepsy: Friend or Foe.Neuroscience bulletin · 2024Review
- MicroRNA205: A Key Regulator of Cardiomyocyte Transition from Proliferative to Hypertrophic Growth in the Neonatal Heart.International journal of molecular sciences · 2024Article
- Pharmacological Targets in Chronic Heart Failure with Reduced Ejection Fraction.Life (Basel, Switzerland) · 2022Review
- Paradoxical roles of caspase-3 in regulating cell survival, proliferation, and tumorigenesis.The Journal of cell biology · 2022Review
- Article
- Potential of Phage Display Antibody Technology for Cardiovascular Disease Immunotherapy.Journal of cardiovascular translational research · 2022Review
- Long noncoding RNA NEAT1 promotes cardiac fibrosis in heart failure through increased recruitment of EZH2 to the Smad7 promoter region.Journal of translational medicine · 2022Article
- Increased Expression of Cardiotrophin-1 in Cardiomyopathy Patients.Balkan journal of medical genetics : BJMG · 2021Article
- Protein kinase CK2: a potential therapeutic target for diverse human diseases.Signal transduction and targeted therapy · 2021Review
- Molecular mechanisms of right ventricular dysfunction in pulmonary arterial hypertension: focus on the coronary vasculature, sex hormones, and glucose/lipid metabolism.Cardiovascular diagnosis and therapy · 2020Review
- The therapeutic impact of human neonatal BMSC in a right ventricular pressure overload model in mice.Stem cell research & therapy · 2020Article
- Regulation of Myocardial Extracellular Matrix Dynamic Changes in Myocardial Infarction and Postinfarct Remodeling.Current cardiology reviews · 2020Review
- Right Atrial Myocardial Remodeling in Children With Atrial Septal Defect Involves Inflammation, Growth, Fibrosis, and Apoptosis.Frontiers in pediatrics · 2020Article
- Druggable Transcriptional Networks in the Human Neurogenic Epigenome.Pharmacological reviews · 2019Review
- Fischer rats exhibit maladaptive structural and molecular right ventricular remodelling in severe pulmonary hypertension: a genetically prone model for right heart failure.Cardiovascular research · 2019Article
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The post-natal heart adapts to stress and overload through hypertrophic growth, a process that may be pathologic or beneficial (physiologic hypertrophy). Physiologic hypertrophy improves cardiac performance in both healthy and diseased individuals, yet the mechanisms that propagate this favorable adaptation remain poorly defined. We identify the cytokine cardiotrophin 1 (CT1) as a factor capable of recapitulating the key features of physiologic growth of the heart including transient and reversible hypertrophy of the myocardium, and stimulation of cardiomyocyte-derived angiogenic signals leading to increased vascularity. The capacity of CT1 to induce physiologic hypertrophy originates from a CK2-mediated restraining of caspase activation, preventing the transition to unrestrained pathologic growth. Exogenous CT1 protein delivery attenuated pathology and restored contractile function in a severe model of right heart failure, suggesting a novel treatment option for this intractable cardiac disease.
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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.