Cross-regulation between the renin-angiotensin system and inflammatory mediators in cardiac hypertrophy and failure

Kenichi Sekiguchi, Xia Li, Mytsi Coker, Markus Flesch, Philip M. Barger, Natarajan Sivasubramanian, Douglas L. Mann

Research output: Contribution to journalReview article

66 Scopus citations

Abstract

One of the major conceptual advances in our understanding of the pathogenesis of heart failure has been the insight that heart failure may progress as the result of the sustained overexpression of biologically active "neurohormones", such as norepinephrine and angiotensin II, which by virtue of their deleterious effects are sufficient to contribute to disease progression by provoking worsening left ventricular (LV) remodeling and progressive LV dysfunction. Recently, a second class of biologically active molecules, termed cytokines, has also been identified in the setting of heart failure. Analogous to the situation with neurohormones, the overexpression of cytokines is sufficient to contribute to disease progression in heart failure phenotype. Although important interactions between proinflammatory cytokines and the adrenergic system have been recognized in the heart for over a decade, the nature of the important interactions between proinflammatory cytokines and the renin-angiotensin system has become apparent only recently. Accordingly, in the present review, we will discuss the evidence which suggests that there is a functionally significant cross-talk between neurohormonal and inflammatory cytokine signaling in cardiac hypertrophy and failure.

Original languageEnglish
Pages (from-to)433-442
Number of pages10
JournalCardiovascular Research
Volume63
Issue number3
DOIs
StatePublished - Aug 15 2004
Externally publishedYes

Keywords

  • Angiotensin II
  • Heart failure
  • Inflammation
  • Renin-angiotensin system
  • Tumor necrosis factor

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