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[Changes in gene expression in terminal myocardial failure].

T Eschenhagen1, U Mende, W Schmitz

  • 1Abteilung Allgemeine Pharmakologie, Universitäts-Krankenhaus Eppendorf, Hamburg.

Zeitschrift Fur Kardiologie
|January 1, 1992
PubMed
Summary

Heart failure involves changes in cardiac gene expression, similar to animal models, impacting heart muscle function. These adaptive changes, while initially beneficial, ultimately worsen heart performance.

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cardiac Pathophysiology

Context:

  • End-stage heart failure is a complex condition often involving myocardial hypertrophy.
  • Animal models reveal adaptive gene expression changes during hypertrophy.

Purpose:

  • To compare gene expression patterns in human end-stage heart failure with experimental cardiac hypertrophy.
  • To investigate the role of gene expression alterations in the progression of heart failure.

Summary:

  • Human heart failure shows parallels with animal models, including decreased SR Ca(2+)-ATPase and phospholamban, and altered beta-adrenoceptor and Gi protein expression.
  • Unlike animal models, human hearts do not exhibit a fetal isoform shift due to pre-existing adult expression.
  • These molecular changes contribute to slowed relaxation and desensitization of the adenylyl cyclase pathway.

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Impact:

  • Suggests that observed gene expression changes in human heart failure are secondary to chronic overload.
  • Highlights that these adaptive responses, initially protective, may ultimately impair myocardial contractility.
  • Provides insights into the molecular mechanisms underlying heart failure progression.