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Cardiovascular Research 2004 63(3):433-442; doi:10.1016/j.cardiores.2004.02.005
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

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

Kenichi Sekiguchia, Xia Lia, Mytsi Cokera, Markus Flescha,b, Philip M Bargera, Natarajan Sivasubramaniana and Douglas L Mann*,a

aCardiology Section of the Department of Medicine, Winters Center for Heart Failure Research, Houston VAMC and Baylor College of Medicine, 6565 Fannin, MS 524, Houston, TX 77030, USA
bKlinik III für Innere Medizin der Universität zu Köln, Cologne, Germany

* Corresponding author. Tel.: +1-713-441-1252; fax: +1-713-441-1246. Email address: dmann{at}bcm.tmc.edu

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.

KEYWORDS Angiotensin II; Renin–angiotensin system; Heart failure; Tumor necrosis factor; Inflammation

Time for primary review 18 days


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