ArticleCirculation2014
c-Cbl inhibition improves cardiac function and survival in response to myocardial ischemia.
Article in Circulation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 29 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
29 citing papers in PubMed, 55 citations in OpenAlex.
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- Integrating lipid-related composite indices and explainable machine learning for coronary heart disease risk assessment.Frontiers in public health · 2026Article
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- Mettl13 protects against cardiac contractile dysfunction by negatively regulating C-Cbl-mediated ubiquitination of SERCA2a in ischemic heart failure.Science China. Life sciences · 2023Article
- CBL knockdown protects cardiomyocytes against hypoxia-reoxygenation injury by downregulating GRB2 expression.Experimental and therapeutic medicine · 2022Article
- Construction of Immune-Related ceRNA Network in Dilated Cardiomyopathy: Based on Sex Differences.Frontiers in genetics · 2022Article
- Identification of Novel and Potent Modulators Involved in Neonatal Cardiac Regeneration.Pediatric cardiology · 2021Article
- MicroRNA-369 attenuates hypoxia-induced cardiomyocyte apoptosis and inflammation via targeting TRPV3.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021Article
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- Loss of Protease-Activated Receptor 4 Prevents Inflammation Resolution and Predisposes the Heart to Cardiac Rupture After Myocardial Infarction.Circulation · 2020Article
- Phosphoproteomic Analysis of Rat Neutrophils Shows the Effect of Intestinal Ischemia/Reperfusion and Preconditioning on Kinases and Phosphatases.International journal of molecular sciences · 2020Article
- Analysis of extracellular vesicle miRNA profiles in heart failure.Journal of cellular and molecular medicine · 2020Article
- Cracking the Monoubiquitin Code of Genetic Diseases.International journal of molecular sciences · 2020Review
- Cellular Protein Quality Control in Diabetic Cardiomyopathy: From Bench to Bedside.Frontiers in cardiovascular medicine · 2020Review
- Effect of moxibustion preconditioning on autophagy-related proteins in rats with myocardial ischemia reperfusion injury.Annals of translational medicine · 2019Article
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- Essential role for smooth muscle cell stromal interaction molecule-1 in myocardial infarction.Journal of hypertension · 2018Article
- High Fat Diet Upregulates Fatty Acid Oxidation and Ketogenesis via Intervention of PPAR-γ.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018Article
Corrections and comments
- Expression of concern · 2023-03-13Concerns/Issues about Data · Concerns/Issues about Image · Investigation by Company/Institution ·
- Expression of concern
Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe proto-oncogene Casitas b-lineage lymphoma (c-Cbl) is an adaptor protein with an intrinsic E3 ubiquitin ligase activity that targets receptor and nonreceptor tyrosine kinases, resulting in their ubiquitination and downregulation. However, the function of c-Cbl in the control of cardiac function is currently unknown. In this study, we examined the role of c-Cbl in myocyte death and cardiac function after myocardial ischemia. METHODS AND
resultsWe show increased c-Cbl expression in human ischemic and dilated cardiomyopathy hearts and in response to pathological stress stimuli in mice. c-Cbl-deficient mice demonstrated a more robust functional recovery after myocardial ischemia/reperfusion injury and significantly reduced myocyte apoptosis and improved cardiac function. Ubiquitination and downregulation of key survival c-Cbl targets, epidermal growth factor receptors and focal adhesion kinase, were significantly reduced in c-Cbl knockout mice. Inhibition of c-Cbl expression or its ubiquitin ligase activity in cardiac myocytes offered protection against H2O2 stress. Interestingly, c-Cbl deletion reduced the risk of death and increased cardiac functional recovery after chronic myocardial ischemia. This beneficial effect of c-Cbl deletion was associated with enhanced neoangiogenesis and increased expression of vascular endothelial growth factor-a and vascular endothelial growth factor receptor type 2 in the infarcted region.
conclusionsc-Cbl activation promotes myocyte apoptosis, inhibits angiogenesis, and causes adverse cardiac remodeling after myocardial infarction. These findings point to c-Cbl as a potential therapeutic target for the maintenance of cardiac function and remodeling after myocardial ischemia.
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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.