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Signalling pathways for cardiac hypertrophy

T Yamazaki1, I Komuro, Y Yazaki

  • 1Third Department of Internal Medicine, Faculty of Medicine, Health Service Center, University of Tokyo, Japan.

Cellular Signalling
|January 12, 1999
PubMed
Summary
This summary is machine-generated.

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Mechanical stretch and neurohumoral factors trigger cardiac hypertrophy. These stimuli activate signaling pathways like extracellular signal-regulated kinases (ERKs) and protein kinases, leading to cardiomyocyte growth.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Signaling

Background:

  • Cardiac hypertrophy is a response to hemodynamic overload, often caused by high blood pressure.
  • Mechanical stretch and neurohumoral factors are key initiators of cardiac hypertrophy.
  • Understanding the signaling pathways involved is crucial for therapeutic development.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying mechanical stretch and neurohumoral factor-induced cardiac hypertrophy.
  • To identify key signaling molecules and pathways involved in cardiomyocyte growth.
  • To differentiate signaling cascades in cardiac myocytes versus cardiac fibroblasts.

Main Methods:

  • The study reviews existing literature on the molecular signaling pathways activated by mechanical stretch and neurohumoral factors in cardiomyocytes.

Related Experiment Videos

  • It focuses on the roles of second messengers, kinases, and growth factors.
  • Comparative analysis of signaling pathways in different cardiac cell types.

    • Main Results:

    • Mechanical stretch activates phosphatidylinositol, protein kinase C, Raf-1 kinase, and extracellular signal-regulated protein kinases (ERKs), promoting protein synthesis.
    • The cardiac renin-angiotensin system and Angiotensin II contribute to pressure-overload hypertrophy via autocrine mechanisms.
    • Specific pathways involving Gbetagamma, Src, Shc, Grb2, Ras, Gq, and protein kinase C are detailed for fibroblasts and myocytes.
    • Mechanical stress also enhances endothelin-1 release and activates the Na+ -H+ exchanger, leading to ERK activation.
    • Norepinephrine activates protein kinase cascades via protein kinase A and protein kinase C.

    Conclusions:

    • Mechanical stretch and neurohumoral factors initiate cardiac hypertrophy through complex signaling cascades.
    • Extracellular signal-regulated kinases (ERKs) and protein kinases play central roles in mediating cardiomyocyte growth.
    • Distinct signaling pathways are employed by different cardiac cell types in response to stimuli.