TY - JOUR
T1 - Future prospects of anticytokine therapy in chronic heart failure
AU - von Haehling, Stephan
AU - Anker, Stefan D.
PY - 2005/2
Y1 - 2005/2
N2 - Several lines of evidence suggest that chronic heart failure is a state of chronic inflammation. Indeed, various pro-inflammatory markers, including the cytokines TNF-α, and interleukin 6 and 1, are activated in the course of the disease. In chronic heart failure, these substances are frequently induced even before the classical neurohormones angiotensin II and noradrenaline. Although the recently published anti-TNF-α trials with etanercept and infliximab have called the beneficial effects of targeting single cytokines into question, the overactive immune system remains a promising target for therapeutic interventions, which aim at slowing down disease progression. Broader approaches are required. These comprise targeting bacterial lipopolysaccharide (endotoxin) that enters the circulation through the oedematous gut wall, immune modulation therapy with patient-derived whole blood exposed to oxidative stress, 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (the so-called statins) and a number of other substances including pentoxifylline and thalidomide.
AB - Several lines of evidence suggest that chronic heart failure is a state of chronic inflammation. Indeed, various pro-inflammatory markers, including the cytokines TNF-α, and interleukin 6 and 1, are activated in the course of the disease. In chronic heart failure, these substances are frequently induced even before the classical neurohormones angiotensin II and noradrenaline. Although the recently published anti-TNF-α trials with etanercept and infliximab have called the beneficial effects of targeting single cytokines into question, the overactive immune system remains a promising target for therapeutic interventions, which aim at slowing down disease progression. Broader approaches are required. These comprise targeting bacterial lipopolysaccharide (endotoxin) that enters the circulation through the oedematous gut wall, immune modulation therapy with patient-derived whole blood exposed to oxidative stress, 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (the so-called statins) and a number of other substances including pentoxifylline and thalidomide.
KW - Heart failure
KW - Immune modulation
KW - Inflammation
KW - Statins
KW - TNF
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U2 - 10.1517/13543784.14.2.163
DO - 10.1517/13543784.14.2.163
M3 - Article
C2 - 15806710
AN - SCOPUS:15544381195
VL - 14
SP - 163
EP - 176
JO - Expert Opinion on Investigational Drugs
JF - Expert Opinion on Investigational Drugs
SN - 1354-3784
IS - 2
ER -