Autocrine and paracrine mechanisms in the pathophysiology of heart failure.
At the cellular and molecular level the transition to heart failure is a complex process that involves structural adaptation, not only of the heart, but of peripheral vasculature and renal tissues as well. Recent studies have suggested that autocrine, paracrine, and circulating biologically active mediators activate events that result in the concerted failure of adaptive mechanisms and the ultimate depression of cardiac myocyte function. Greater understanding of these local mechanisms in the future may lead to drug therapies that can selectively block these mechanisms and prevent the progression from compensation to overt heart failure.
Dzau
V J
VJ
Falk Cardiovascular Research Center, Stanford University School of Medicine, California 94305-5246.
D006332:Cardiomegaly / Q000473:pathology* / Q000503:physiopathology*; D006321:Heart / Q000503:physiopathology*; D006333:Heart Failure / Q000473:pathology* / Q000503:physiopathology*; D006801:Humans; D009490:Neurosecretory Systems / Q000473:pathology* / Q000503:physiopathology*; D018377:Neurotransmitter Agents / Q000502:physiology
D018377:Neurotransmitter Agents