ArticleJournal of molecular and cellular cardiology2010
Tumor necrosis factor-alpha produced in cardiomyocytes mediates a predominant myocardial inflammatory response to stretch in early volume overload.
Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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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
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Neutropenic Enterocolitis and Sepsis: Towards the Definition of a Pathologic Profile.Medicina (Kaunas, Lithuania) · 2021Pooled it
- Microfluidic Modeling of Macrophage-Induced Cardiac Inflammation Using NF-κB Reporter Cardiomyocytes.Advanced healthcare materials · 2026Article
- Targeted delivery of TAPI-1 via biomimetic nanoparticles ameliorates post-infarct left ventricle function and remodelling.Cardiovascular research · 2025Article
- Heart-specific NFAT5 knockout suppresses type I interferon signaling and aggravates coxsackievirus-induced myocarditis.Basic research in cardiology · 2024Article
- Neutral sphingomyelinase regulates mechanotransduction in human engineered cardiac tissues and mouse hearts.The Journal of physiology · 2024Article
- Adipocyte-released adipomes in Chagas cardiomyopathy: Impact on cardiac metabolic and immune regulation.iScience · 2024Article
- Differential cardiomyocyte transcriptomic remodeling during in vitro Trypanosoma cruzi infection using laboratory strains provides implications on pathogenic host responses.Tropical medicine and health · 2023Article
- COVID-19 and the cardiovascular system: an update.The American journal of the medical sciences · 2022Review
- Necroptosis in heart disease: Molecular mechanisms and therapeutic implications.Journal of molecular and cellular cardiology · 2022Review
- Role of platelet rich plasma mediated repair and regeneration of cell in early stage of cardiac injury.Regenerative therapy · 2022Review
- Left Ventricular Remodeling in Non-syndromic Mitral Valve Prolapse: Volume Overload or Concomitant Cardiomyopathy?Frontiers in cardiovascular medicine · 2022Review
- Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling.Scientific reports · 2021Article
- Mechanisms of COVID-19-induced heart failure: a short review.Heart failure reviews · 2021Review
- Cardiac remodeling secondary to chronic volume overload is attenuated by a novel MMP9/2 blocking antibody.PloS one · 2020Article
- Programmed necrosis in cardiomyocytes: mitochondria, death receptors and beyond.British journal of pharmacology · 2019Review
- Soybean glycinin decreased growth performance, impaired intestinal health, and amino acid absorption capacity of juvenile grass carp (Ctenopharyngodon idella).Fish physiology and biochemistry · 2019Article
- Inflammation in myocardial injury: mesenchymal stem cells as potential immunomodulators.American journal of physiology. Heart and circulatory physiology · 2019Review
- Fibroblasts in the Infarcted, Remodeling, and Failing Heart.JACC. Basic to translational science · 2019Review
- Longitudinal changes of cardiac troponin and inflammation reflect progressive myocyte stretch and likelihood for hypertension in a Black male cohort: The SABPA study.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Article
- Galanin receptor 2 mediates antifibrogenic effects of galanin on hepatic stellate cells.Experimental and therapeutic medicine · 2016Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Acute stretch caused by volume overload (VO) of aorto-caval fistula (ACF) induces a variety of myocardial responses including mast cell accumulation, matrix metalloproteinase (MMP) activation, and collagen degradation, all of which are critical in dictating long-term left ventricle (LV) outcome to VO. Meanwhile, these responses can be part of myocardial inflammation dictated by tumor necrosis factor-alpha (TNF-alpha), which is elevated after acute ACF. However, it is unknown whether TNF-alpha mediates a major myocardial inflammatory response to stretch in early VO. In 24-h ACF and sham rats, microarray gene expression profiling and subsequent Ingenuity Pathway Analysis identified a predominant inflammatory response and a gene network of biologically interactive genes strongly linked to TNF-alpha. Western blot demonstrated increased local production of TNF-alpha in the LV (1.71- and 1.66-fold in pro- and active-TNF-alpha over control, respectively, P<0.05) and cardiomyocytes (2- and 4-fold in pro- and active-TNF-alpha over control, respectively, P<0.05). TNF-alpha neutralization with infliximab (5.5 mg/kg) attenuated the myocardial inflammatory response to acute VO, as indicated by inhibition of inflammatory gene upregulation, myocardial infiltration (total CD45+ cells, mast cells, and neutrophils), MMP-2 activation, collagen degradation, and cardiac cell apoptosis, without improving LV remodeling and function. These results indicate that TNF-alpha produced by cardiomyocytes mediates a predominant inflammatory response to stretch in the early VO in the ACF rat, suggesting an important role of TNF-alpha in initiating pathophysiological response of myocardium to VO.
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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.