ArticleJournal of cellular and molecular medicine2010
TNF-alpha-mediated signal transduction pathway is a major determinant of apoptosis in dilated cardiomyopathy.
Article in Journal of cellular and molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- TongGuanWan Alleviates Doxorubicin- and Isoproterenol-Induced Cardiac Hypertrophy and Fibrosis by Modulating Apoptotic and Fibrotic Pathways.International journal of molecular sciences · 2024Article
- Article
- Machine learning and bioinformatics to identify 8 autophagy-related biomarkers and construct gene regulatory networks in dilated cardiomyopathy.Scientific reports · 2022Article
- Article
- TotalCardiovascular diagnosis and therapy · 2019Article
- ERK1/2 communicates GPCR and EGFR signaling pathways to promote CTGF-mediated hypertrophic cardiomyopathy upon Ang-II stimulation.BMC molecular and cell biology · 2019Article
- Role of cytokines and inflammation in heart function during health and disease.Heart failure reviews · 2018Review
- Suppression of phosphorylated MAPK and caspase 3 by carbon dioxide.Molecular and cellular biochemistry · 2017Article
- Longitudinal observations of progressive cardiac dysfunction in a cardiomyopathic animal model by self-gated cine imaging based on 11.7-T magnetic resonance imaging.Scientific reports · 2017Article
- Knockdown of embryonic myosin heavy chain reveals an essential role in the morphology and function of the developing heart.Development (Cambridge, England) · 2011Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Although J2N-k strain of cardiomyopathic hamsters is an excellent model of dilated cardiomyopathy, the presence and mechanisms of apoptosis in the hearts of these genetically modified animals have not been investigated. This study examined the hypothesis that cardiac dysfunction and apoptosis in the cardiomyopathic hamsters were associated with tumour necrosis factor-alpha (TNF-alpha)-mediated signalling pathway involving the activation of some pro-apoptotic proteins and/or deactivation of some antiapoptotic proteins. Echocardiographic assessment of 31-week-old hamsters indicated an increase in the internal dimension of the left ventricle as well as decreases in the ejection fraction, fractional shortening and cardiac output without any evidence of cardiac hypertrophy. Increased level of TNF-alpha and apoptosis in cardiomyopathic hearts were accompanied by increased protein content for protein kinase C (PKC) -alpha and -epsilon isozymes as well as caspases 3 and 9. Phosphorylated protein content for p38 MAPK and NF kappaB was increased whereas that for Erk1/2, BAD and Bcl-2 was decreased in cardiomyopathic hearts. These results support the view that TNF-alpha and PKC isozymes may promote apoptosis due to the activation of p38 MAPK and deactivation of Erk1/2 pathways, and these changes may contribute toward the development of cardiac dysfunction in dilated cardiomyopathy.
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Registered trials
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