Reversing advanced heart failure by targeting Ca2+ cycling.
Heart failure is a major cardiovascular disease, characterized by considerable morbidity and mortality. Despite major advances in the pharmacotherapy of heart failure, the options for patients with severe end-stage symptoms remain limited. However, recent developments in the identification of the molecular basis for the progressive nature of heart failure have identified a number of potentially important new therapeutic targets. In particular, key components of the cardiomyocyte calcium-handling pathway show characteristic changes in heart failure. A body of research examining the effect of restoration of these defects in experimental models of heart failure, whether in genetically engineered mouse models or by myocardial gene transfer, very strongly supports the calcium-handling pathway as a target for clinical intervention.
Kaye
David M
DM
Heart Failure Research Group, Baker Heart Research Institute, Melbourne, Victoria 8008, Australia. david.kaye@baker.edu.au
Hoshijima
Masahiko
M
Chien
Kenneth R
KR
D002121:Calcium Channel Blockers; D015220:Calcium Channels / Q000502:physiology*; D020013:Calcium Signaling / Q000502:physiology*; D015316:Genetic Therapy; D006333:Heart Failure / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; C506946:ATP2A2 protein, human