Cytokines and cardiac hypertrophy: roles of angiotensin II and basic fibroblast growth factor

Clin Exp Pharmacol Physiol Suppl. 1996;3:S136-41.


1. While the haemodynamic influences that cause cardiac hypertrophy are well known, the cellular and molecular mechanisms by which a mechanical stimulus is translated into a growth response by cardiac muscle have remained uncertain. 2. Current evidence suggests that a number of trophic factors may be released by cellular constituents of the heart, acting in an autocrine or paracrine manner to influence the growth response and phenotype of neighbouring cells. 3. Angiotensin II, acting via the AT1 receptor subtype, and both basic fibroblast growth factor and heparin-binding epidermal growth factor have been shown to exert hypertrophic actions in vivo and in vitro. Studies also indicate that cardiac myocytes themselves are capable of releasing all of these cytokines in response to increased mechanical load.

Publication types

  • Congress
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Angiotensin II / adverse effects
  • Angiotensin II / metabolism*
  • Animals
  • Cardiomegaly / etiology*
  • Cardiomegaly / physiopathology
  • Epidermal Growth Factor / adverse effects
  • Epidermal Growth Factor / metabolism*
  • Fibroblast Growth Factors / adverse effects
  • Fibroblast Growth Factors / metabolism*
  • Heart / drug effects
  • Heparin / metabolism
  • Heparin-binding EGF-like Growth Factor
  • Intercellular Signaling Peptides and Proteins
  • Molecular Weight
  • Myocardium / cytology
  • Myocardium / metabolism
  • Phenotype
  • Receptors, Angiotensin / drug effects


  • Heparin-binding EGF-like Growth Factor
  • Intercellular Signaling Peptides and Proteins
  • Receptors, Angiotensin
  • Angiotensin II
  • Fibroblast Growth Factors
  • Epidermal Growth Factor
  • Heparin