ArticleCirculation. Heart failure2013
Tumor necrosis factor receptor-associated factor 2 signaling provokes adverse cardiac remodeling in the adult mammalian heart.
Article in Circulation. Heart failure, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- The Role of CD147 in Pathological Cardiac Hypertrophy Is Regulated by Glycosylation.Oxidative medicine and cellular longevity · 2022Article
- Tumor Necrosis Factor-α in Heart Failure: an Updated Review.Current cardiology reports · 2018Review
- Article
- The Role of the Mammalian Target of Rapamycin (mTOR) in Pulmonary Fibrosis.International journal of molecular sciences · 2018Review
- TNF receptor-activated factor 2 mediates cardiac protection through noncanonical NF-κB signaling.JCI insight · 2018Article
- TRAF molecules in inflammation and inflammatory diseases.Current pharmacology reports · 2018Article
- G3BP2 is involved in isoproterenol-induced cardiac hypertrophy through activating the NF-κB signaling pathway.Acta pharmacologica Sinica · 2018Article
- Emergence of Members of TRAF and DUB of Ubiquitin Proteasome System in the Regulation of Hypertrophic Cardiomyopathy.Frontiers in genetics · 2018Review
- Impaired Protein Quality Control During Left Ventricular Remodeling in Mice With Cardiac Restricted Overexpression of Tumor Necrosis Factor.Circulation. Heart failure · 2017Article
- T helper cells with specificity for an antigen in cardiomyocytes promote pressure overload-induced progression from hypertrophy to heart failure.Scientific reports · 2017Article
- Cardioprotective Role of Tumor Necrosis Factor Receptor-Associated Factor 2 by Suppressing Apoptosis and Necroptosis.Circulation · 2017Article
- Proinflammatory Cytokines Mediate GPCR Dysfunction.Journal of cardiovascular pharmacology · 2017Review
- Recent advances of adapter proteins in the regulation of heart diseases.Heart failure reviews · 2017Review
- The ubiquitin E3 ligase TRAF6 exacerbates pathological cardiac hypertrophy via TAK1-dependent signalling.Nature communications · 2016Article
- Functional significance of the discordance between transcriptional profile and left ventricular structure/function during reverse remodeling.JCI insight · 2016Article
- Necrotic myocardial cells release damage-associated molecular patterns that provoke fibroblast activation in vitro and trigger myocardial inflammation and fibrosis in vivo.Journal of the American Heart Association · 2015Article
- Tumor necrosis factor receptor-associated factor 2 mediates mitochondrial autophagy.Circulation. Heart failure · 2015Article
- Catechin ameliorates cardiac dysfunction in rats with chronic heart failure by regulating the balance between Th17 and Treg cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
- Dysferlin mediates the cytoprotective effects of TRAF2 following myocardial ischemia reperfusion injury.Journal of the American Heart Association · 2014Article
- TWEAK-Fn14 Cytokine-Receptor Axis: A New Player of Myocardial Remodeling and Cardiac Failure.Frontiers in immunology · 2014Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTumor necrosis factor superfamily ligands provoke a dilated cardiac phenotype signal through a common scaffolding protein termed tumor necrosis factor receptor-associated factor 2 (TRAF2); however, virtually nothing is known about TRAF2 signaling in the adult mammalian heart. METHODS AND
resultsWe generated multiple founder lines of mice with cardiac-restricted overexpression of TRAF2 and characterized the phenotype of mice with higher expression levels of TRAF2 (myosin heavy chain [MHC]-TRAF2(HC)). MHC-TRAF2(HC) transgenic mice developed a time-dependent increase in cardiac hypertrophy, left ventricular dilation, and adverse left ventricular remodeling, and a significant decrease in LV+dP/dt and LV-dP/dt when compared with littermate controls (P<0.05 compared with littermate). During the early phases of left ventricular remodeling, there was a significant increase in total matrix metalloproteinase activity that corresponded with a decrease in total myocardial fibrillar collagen content. As the MHC-TRAF2(HC) mice aged, there was a significant decrease in total matrix metalloproteinase activity accompanied by an increase in total fibrillar collagen content and an increase in myocardial tissue inhibitor of metalloproteinase-1 levels. There was a significant increase in nuclear factor-κB activation at 4 to 12 weeks and jun N-terminal kinases activation at 4 weeks in the MHC-TRAF2(HC) mice. Transciptional profiling revealed that >95% of the hypertrophic/dilated cardiomyopathy-related genes that were significantly upregulated genes in the MHC-TRAF2(HC) hearts contained κB elements in their promoters.
conclusionsThese results show for the first time that targeted overexpression of TRAF2 is sufficient to mediate adverse cardiac remodeling in the heart.
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