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Reversing advanced heart failure by targeting Ca2+ cycling
David M Kaye1, Masahiko Hoshijima, Kenneth R Chien
1Heart Failure Research Group, Baker Heart Research Institute, Melbourne, Victoria 8008, Australia. david.kaye@baker.edu.au
Annual Review of Medicine
|January 12, 2008
Summary
Heart failure remains a significant cardiovascular disease with limited treatment options for severe cases. Targeting the cardiomyocyte calcium-handling pathway shows promise for developing new heart failure therapies.
Area of Science:
- Cardiovascular Medicine
- Molecular Biology
- Genetics
Background:
- Heart failure (HF) is a leading cause of cardiovascular morbidity and mortality.
- Current pharmacotherapy for HF has limitations, especially for end-stage patients.
- Recent research has identified molecular targets for progressive heart failure.
Purpose of the Study:
- To investigate the role of cardiomyocyte calcium-handling pathway defects in heart failure.
- To evaluate the therapeutic potential of targeting these defects.
Main Methods:
- Analysis of molecular basis of progressive heart failure.
- Examination of cardiomyocyte calcium-handling pathway alterations in heart failure models.
- Studies in genetically engineered mouse models of heart failure.
- Myocardial gene transfer techniques in experimental models.
Main Results:
- Characteristic changes in the cardiomyocyte calcium-handling pathway are observed in heart failure.
- Restoration of these calcium-handling defects in experimental models shows therapeutic promise.
- Evidence strongly supports the calcium-handling pathway as a viable clinical intervention target.
Conclusions:
- The cardiomyocyte calcium-handling pathway is a critical area for therapeutic development in heart failure.
- Targeting molecular defects, particularly in calcium handling, offers a promising strategy for future heart failure treatments.
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