Cytokines and heart failure

Cardiol Rev. Jul-Aug 1999;7(4):196-206. doi: 10.1097/00045415-199907000-00011.

Abstract

The current interest in understanding the role of stress-induced cytokines in heart failure relates to the observation that many of the untoward pathophysiologic responses of the failing circulation might be explained by these compounds. These small molecules appear to cause left ventricular dysfunction, precipitate pulmonary edema, cause cardiomyopathy, reduce peripheral organ perfusion, induce ventricular remodeling, activate the fetal gene program in animal models, and cause anorexia and cachexia. Thus, the elaboration of cytokines, similar to the upregulation of neurohormones, may represent a biochemical mechanism that is responsible for producing symptoms and remodeling in heart failure patients. To better understand how cytokines play a role in heart failure, it is important to delineate the concept of cytokine bioactivity in this setting.

Publication types

  • Review

MeSH terms

  • Cytokines / biosynthesis*
  • Female
  • Heart Failure / epidemiology
  • Heart Failure / etiology*
  • Heart Failure / metabolism
  • Humans
  • Incidence
  • Interferons / biosynthesis
  • Male
  • Risk Assessment
  • Sensitivity and Specificity
  • Survival Rate
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Cytokines
  • Tumor Necrosis Factor-alpha
  • Interferons