ErbB2 is essential in the prevention of dilated cardiomyopathy

By Steven A. Crone, You-yang Zhao, Lian Fan, Yusu Gu, S. Minamisawa, Yang Liu, K. Peterson, Ju Chen, R. Kahn, G. Condorelli and 3 more. Nature Medicine, 2002

886 citations recorded by the source corpus.

Subfields: Immunology and Allergy, Oncology, Radiology, Nuclear Medicine and Imaging

View Paper: https://www.semanticscholar.org/paper/f20e0f352f52615dac1f9e489eac2465e762a069

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In Immunology and Allergy

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Citations in the corpus

ErbB receptors: directing key signaling networks throughout life. (2004, background): “However, starting at approximately eight weeks, they develop severe dilated cardiomyopathy, resulting in reduced contractile function of the heart (79, 80).”
Regulation of cardiac hypertrophy by intracellular signalling pathways (2006, background): “, as well as the cardiac-specific deletion of ERBB2 both lead to cardiomyopathy, showing the critical importance of this signalling effector in the maintenance of myocyte integrity and growt”
The safety and side effects of monoclonal antibodies (2010, background): “Mice with cardiac-specific deletion of ERBB2 develop age-related dilated cardiomyopathy, characterized by the presence of cardiac myocytes with increased numbers of mitochondria, vacuoles and sensitivity to anthracycline”
Anthracycline Chemotherapy and Cardiotoxicity (2017, background): “This leads to compensatory cellular hypertrophy, whereas deletion models demonstrate dilated cardiomyopathy and systolic dysfunction in the presence of pressure overload [28].”
The epidermal growth factor receptor family: Biology driving targeted therapeutics (2008, background): “Consistent with the cardiomyopathy seen in mice lacking myocardial ErbB2 [121,122], one complication of trastuzumab is the development of a reversible cardiomyopathy often with congestive heart failure in approximately 3 % of patients [168].”
Model organisms: The mighty mouse: genetically engineered mouse models in cancer drug development (2006, positive): “Germline Her2/neu -knockout mice are not viable, and the mechanism of this toxicity has instead been recently explained through the use of a GEMM with tissue-specific inactivation of HER2/ neu in the hear”
TACE is required for fetal murine cardiac development and modeling. (2003, background): “In contrast, null mutations in several other genes, such as heparin-binding epidermal growth factor (HB-EGF), ErbB2, HOP, PTEN, and phospholamban, result in myocardial hyperplasia, and/or hypertrophy as well as reduced contractile function (Iwamoto et al., 2003; Ozcelik et al., 2002; Crone et al., 2”
Disease candidate gene identification and prioritization using protein interaction networks (2009, background): “Mining the "clinical synopsis" and "allelic variant sections" of NCBI's OMIM (Online Mendelian Inheritance in Man) database [49], we extracted 166 OMIM records that had the terms "atrial septal defect" OR "ASD" OR "ventricular septal defect" OR "VSD" occurring in the text.”
Cardiovascular complications of cancer therapy: incidence, pathogenesis, diagnosis, and management. (2009, background): “Cardiotoxicity caused by trasuzumab is most likely secondary to inhibition of cardiomycyte human epidermal growth factor receptor 2, also nown as ErbB2 signaling, thereby interfering with normal rowth, repair, and survival of cardiomyocytes (22,41,42).”
Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition (2007, background): “Mice with cardiac-specific deletion of Erbb2 late in development are viable, but develop age-related dilated cardiomyopathy and have decreased survival after pressure overload stress , which mimics severe hypertensio”