Heart failure is a major healthcare problem and leading cause of death in Western countries. Growing evidence has shown recent improvements in pharmacological therapy, such as receptor-regulating agents, in treating heart failure; however, the morbidity and mortality of heart failure is still high. More recent studies have suggested the presence of additional molecular targets for treating heart failure. Several key molecules in the beta adrenergic receptor signaling pathway play an important role in the progression of heart failure, and transgenic mice studies supported beneficial effects of controlling such molecules in heart failure. In addition, molecules in the renin-angiotensin system or calcium signaling pathway may also be potential targets for treating heart failure. In this review, we focused on putative mechanisms underlying the beneficial effects of regulating these molecules on the progression of heart failure including relevant patents on this topic.
Keywords: Adenylyl cyclase, βARK1, βARK-CT, DAA-I, angiotensin-(1-7), ASK1, MST-1, FADD, JTV519e, αMHC
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