Tumor Necrosis Factor-α Mediates Cardiac Remodeling and Ventricular Dysfunction After Pressure Overload State
| العنوان: | Tumor Necrosis Factor-α Mediates Cardiac Remodeling and Ventricular Dysfunction After Pressure Overload State |
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| المؤلفون: | Malcolm Arnold, Jeff Y. Li, Lorrie A. Kirshenbaum, Fayez Dawood, Peter P. Liu, Thomas S. Parker, Manyin Chen, Mei Sun, Zamaneh Kassiri, Urszula Zurawska, Rama Khokha |
| المصدر: | Circulation. 115:1398-1407 |
| بيانات النشر: | Ovid Technologies (Wolters Kluwer Health), 2007. |
| سنة النشر: | 2007 |
| مصطلحات موضوعية: | Male, Mechanical overload, medicine.medical_specialty, Cardiomyopathy, Apoptosis, Muscle hypertrophy, Mice, Ventricular Dysfunction, Left, Ventricular hypertrophy, Physiology (medical), Internal medicine, Ventricular Pressure, medicine, Animals, Myocytes, Cardiac, RNA, Messenger, Ventricular remodeling, Aorta, Cells, Cultured, Mice, Knockout, Pressure overload, Ventricular Remodeling, Tumor Necrosis Factor-alpha, business.industry, Myocardium, Cardiac myocyte, medicine.disease, Fibrosis, Mice, Inbred C57BL, Disease Models, Animal, Myocarditis, Endocrinology, Matrix Metalloproteinase 9, Heart failure, cardiovascular system, Cardiology, Hypertrophy, Left Ventricular, Cardiology and Cardiovascular Medicine, business |
| الوصف: | Background— Pressure overload is accompanied by cardiac myocyte apoptosis, hypertrophy, and inflammatory/fibrogenic responses that lead to ventricular remodeling and heart failure. Despite incomplete understanding of how this process is regulated, the upregulation of tumor necrosis factor (TNF)-α after aortic banding in the myocardium is known. In the present study, we tested our hypothesis that TNF-α regulates the cardiac inflammatory response, extracellular matrix homeostasis, and ventricular hypertrophy in response to mechanical overload and contributes to ventricular dysfunction. Methods and Results— C57/BL wild-type mice and TNF-knockout (TNF −/− ) mice underwent descending aortic banding or sham operation. Compared with sham-operated mice, wild-type mice with aortic banding showed a significant increase in cardiac TNF-α levels, which coincided with myocyte apoptosis, inflammatory response, and cardiac hypertrophy in week 2 and a significant elevation in matrix metalloproteinase-9 activity and impaired cardiac function in weeks 2 and 6. Compared with wild-type mice with aortic banding, TNF −/− mice with aortic banding showed attenuated cardiac apoptosis, hypertrophy, inflammatory response, and reparative fibrosis. These mice also showed reduced cardiac matrix metalloproteinase-9 activity and improved cardiac function. Conclusions— Findings from the present study have suggested that TNF-α contributes to adverse left ventricular remodeling during pressure overload through regulation of cardiac repair and remodeling, leading to ventricular dysfunction. |
| تدمد: | 1524-4539 0009-7322 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ff8b1a3a32d180e467637ee609540467Test https://doi.org/10.1161/circulationaha.106.643585Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....ff8b1a3a32d180e467637ee609540467 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15244539 00097322 |
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