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机构地区:[1]中国人民解放军总医院老年心血管病研究所,北京100853
出 处:《基础医学与临床》2000年第3期5-9,共5页Basic and Clinical Medicine
摘 要:Chronic heart failure(CHF ) occurs when abnormality of cardiac function causes the heart to fail to pump bloodat a rate required by the metabolising tissue. CHF is highly complex disorders that arise as a result of combination of genetic,pathophysiologic, and environmental factors. Cellular transduction plays an important role in the pathogenesis of CHF andmany signaling molecules, rebeptors, and intracellular signaling paths are involved. Peptide hormones, growth factors, andcytokines can activate heteromeric (Gq ) or low-molecular-weight guanosine triphosphate (GTP) -binding protein (ras ), andthe transmembrane signal transducer gp130 and induce CHF respectively. Recently it is reported that calcineurin (a Ca2+/calmodulin dependent phosphoprotein phosphatase) plays a significant role in myocyte hypertrophy and heart failure. Thepresent article reviews the progress in cellular signal transduction mechanisms in CHF.Chronic heart failure(CHF ) occurs when abnormality of cardiac function causes the heart to fail to pump bloodat a rate required by the metabolising tissue. CHF is highly complex disorders that arise as a result of combination of genetic,pathophysiologic, and environmental factors. Cellular transduction plays an important role in the pathogenesis of CHF andmany signaling molecules, rebeptors, and intracellular signaling paths are involved. Peptide hormones, growth factors, andcytokines can activate heteromeric (Gq ) or low-molecular-weight guanosine triphosphate (GTP) -binding protein (ras ), andthe transmembrane signal transducer gp130 and induce CHF respectively. Recently it is reported that calcineurin (a Ca2+/calmodulin dependent phosphoprotein phosphatase) plays a significant role in myocyte hypertrophy and heart failure. Thepresent article reviews the progress in cellular signal transduction mechanisms in CHF.
分 类 号:R541.6[医药卫生—心血管疾病]
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