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Hypertension, cardiotrophin-1 and gp130: three points to heart failure?

Heart failure is a chronic condition that is a leading cause of death in the developed western world and results from any structural or functional disorder that impairs contractile performance. The transition of the ventricular myocardium from a healthy, vital organ to a decompensated, failing one is complex and is frequently the result of multiple factors such as underlying hypertension, coronary arterial disease, acute injury (as with myocardial infarction), fibrosis, biomechanical stress, hypertrophy and cardiomyocyte apoptosis [1]. Efforts to understand the complex biological signaling underlying the development and evolution of heart failure have resulted in the identification of a multiplicity of circulating and tissuebased neurohumoral factors such as the renin–angiotensin system, aldosterone, endothelin, tumor necrosis factor-a, the natriuretic peptides and adrenomedullin [2]. All of these factors activate cellular receptors, which in turn stimulate intracellular cardiomyocyte kinase pathways such as Jak-STAT, p42/p44 mitogen-activated protein (MAPK) and phosphatidylinositol-3/protein kinase B (PI3K-Akt), to signal, in broad terms, either survival or destruction of the myocyte [3]. A relatively new player in this system is the gp130/gp190 [leukemia inhibitory factor (LIF)] receptor system, which is stimulated by the interleukin (IL)-6 family of cytokines [4].