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Role of proto-oncogenes in myocardial hypertrophy

A question of major clinical significance in cardiology is the nature of the signals that initiate and maintain the various types of myocardial hypertrophy, either in response to hemodynamic loading or in the absence of altered load. This review suggests that the proto-oncogene model, a concept deri... Full description

Journal Title: The American journal of cardiology 1988, Vol.62 (11), p.13-19
Main Author: Simpson, Paul C
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: United States: Elsevier Inc
ID: ISSN: 0002-9149
Link: https://www.ncbi.nlm.nih.gov/pubmed/2972186
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title: Role of proto-oncogenes in myocardial hypertrophy
format: Article
creator:
  • Simpson, Paul C
subjects:
  • Abridged Index Medicus
  • Cardiomegaly - physiopathology
  • Cells, Cultured
  • DNA Replication
  • Growth Substances - physiology
  • Humans
  • Models, Biological
  • Myocardium - cytology
  • Proto-Oncogenes
  • RNA, Messenger
  • Transcription Factors - physiology
  • Transcription, Genetic
ispartof: The American journal of cardiology, 1988, Vol.62 (11), p.13-19
description: A question of major clinical significance in cardiology is the nature of the signals that initiate and maintain the various types of myocardial hypertrophy, either in response to hemodynamic loading or in the absence of altered load. This review suggests that the proto-oncogene model, a concept derived from the study of cancer, can be very useful in identifying these signals. The proto-oncogene model conceives of cell growth regulation in terms of a limited number of classes of critical regulatory proteins: growth factors, growth factor receptors, intracellular transducing proteins and ribonucleic acid (RNA) transcription factors. Growth of all cells has dissociable components: hypertrophy (growth in size), deoxyribonucleic acid synthesis, mitosis and cytokinesis. Hypertrophy may be the end result of activation of RNA transcription. The various types of hypertrophy could reflect transcription of specific myocyte genes in response to different growth factors. At least 1 member of each functional class of proto-oncogenes has been detected in the myocardium or myocytes, or both. The α 1-adrenergic receptor has been shown to be a growth factor receptor and to regulate RNA transcription. Continued work on proto-oncogenes in myocytes may open the way to manipulate the growth of these cells.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0002-9149
fulltext: fulltext
issn:
  • 0002-9149
  • 1879-1913
url: Link


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descriptionA question of major clinical significance in cardiology is the nature of the signals that initiate and maintain the various types of myocardial hypertrophy, either in response to hemodynamic loading or in the absence of altered load. This review suggests that the proto-oncogene model, a concept derived from the study of cancer, can be very useful in identifying these signals. The proto-oncogene model conceives of cell growth regulation in terms of a limited number of classes of critical regulatory proteins: growth factors, growth factor receptors, intracellular transducing proteins and ribonucleic acid (RNA) transcription factors. Growth of all cells has dissociable components: hypertrophy (growth in size), deoxyribonucleic acid synthesis, mitosis and cytokinesis. Hypertrophy may be the end result of activation of RNA transcription. The various types of hypertrophy could reflect transcription of specific myocyte genes in response to different growth factors. At least 1 member of each functional class of proto-oncogenes has been detected in the myocardium or myocytes, or both. The α 1-adrenergic receptor has been shown to be a growth factor receptor and to regulate RNA transcription. Continued work on proto-oncogenes in myocytes may open the way to manipulate the growth of these cells.
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subjectAbridged Index Medicus ; Cardiomegaly - physiopathology ; Cells, Cultured ; DNA Replication ; Growth Substances - physiology ; Humans ; Models, Biological ; Myocardium - cytology ; Proto-Oncogenes ; RNA, Messenger ; Transcription Factors - physiology ; Transcription, Genetic
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abstractA question of major clinical significance in cardiology is the nature of the signals that initiate and maintain the various types of myocardial hypertrophy, either in response to hemodynamic loading or in the absence of altered load. This review suggests that the proto-oncogene model, a concept derived from the study of cancer, can be very useful in identifying these signals. The proto-oncogene model conceives of cell growth regulation in terms of a limited number of classes of critical regulatory proteins: growth factors, growth factor receptors, intracellular transducing proteins and ribonucleic acid (RNA) transcription factors. Growth of all cells has dissociable components: hypertrophy (growth in size), deoxyribonucleic acid synthesis, mitosis and cytokinesis. Hypertrophy may be the end result of activation of RNA transcription. The various types of hypertrophy could reflect transcription of specific myocyte genes in response to different growth factors. At least 1 member of each functional class of proto-oncogenes has been detected in the myocardium or myocytes, or both. The α 1-adrenergic receptor has been shown to be a growth factor receptor and to regulate RNA transcription. Continued work on proto-oncogenes in myocytes may open the way to manipulate the growth of these cells.
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