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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Endothelial expression of hypoxia-inducible factor 1 protects the murine heart and aorta from pressure overload by suppression of TGF-β signaling
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Endothelial expression of hypoxia-inducible factor 1 protects the murine heart and aorta from pressure overload by suppression of TGF-β signaling

机译:内皮细胞缺氧诱导因子1的表达通过抑制TGF-β信号传导,保护小鼠心脏和主动脉免于压力超负荷

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摘要

In patients with hypertension, increased blood pressure forces the heart to pum p against increased resistance. The heart adapts by increasing the muscle mass of the left ventricle, which then consumes increased amounts of O_2. The resulting O_2 deprivation, or hypoxia, stimulates the formation of new blood vessels in a process known as angiogenesis. Heart function declines when O_2 delivery (through angiogenesis) does not keep up with O_2 demand (from hypertrophy). Hypoxiainducible factor 1 (HIF-1) is a transcription factor that mediates angiogenesis (1). This response pathway may be impaired in patients with hypertension who develop heart failure.
机译:在患有高血压的患者中,血压升高会迫使心脏抵抗阻力的增加。心脏通过增加左心室的肌肉质量来适应,然后消耗更多的O_2。导致的O_2剥夺或缺氧会在称为血管生成的过程中刺激新血管的形成。当O_2输送(通过血管生成)不能满足O_2需求(来自肥大)时,心脏功能就会下降。低氧诱导因子1(HIF-1)是介导血管生成的转录因子(1)。在患有心力衰竭的高血压患者中,该反应途径可能受损。

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    Vascular Program, Institute for Cell Engineering,McKusick-Nathans Institute of Genetic Medicine;

    Departments of Molecular and Comparative Pathobiology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205;

    Departments of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205;

    Departments of Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21205;

    Vascular Program, Institute for Cell Engineering,McKusick-Nathans Institute of Genetic Medicine;

    Departments of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205;

    Departments of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205;

    Vascular Program, Institute for Cell Engineering,McKusick-Nathans Institute of Genetic Medicine;

    Departments of Molecular and Comparative Pathobiology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205;

    Departments of Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21205;

    McKusick-Nathans Institute of Genetic Medicine,Departments of Pediatrics, The Johns Hopkins University School of Medicine, Baltimore, MD 21205;

    Departments of Molecular and Comparative Pathobiology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205;

    Departments of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205;

    Vascular Program, Institute for Cell Engineering,McKusick-Nathans Institute of Genetic Medicine,Departments of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205,Departments of Pediatrics, The Johns Hopkins University School of Medicine, Baltimore, MD 21205,Departments of Oncology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205,Departments of Radiation Oncology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205,Departments of Biological Chemistry The Johns Hopkins University School of Medicine, Baltimore, MD 21205;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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