Why the study?
Do therapies targeting sarcoplasmic reticulum function improve cardiac performance in heart disease?
Do therapies targeting sarcoplasmic reticulum function improve cardiac performance in heart disease?
This review highlights the sarcoplasmic reticulum as a key therapeutic target in heart disease, noting that existing therapies like beta-blockers and ACE inhibitors exert beneficial effects partly through SR function improvement.
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May support sarcoplasmic reticulum modulation in heart failure therapy; leaves open dedicated trials before practice change.
The sarcoplasmic reticulum (SR) is a major player in maintaining cardiac function, as it is intimately involved in the regulation of Ca2+-movements on a beat-to-beat basis. SR dysfunction due to abnormalities in SR protein content has been reported in different cardiac diseases such as ischaemic heart disease, myocardial infarction, congestive heart failure and various cardiomyopathies; thus the genes expressing the SR Ca2+-pump, Ca2+-channels, calsequestrin, phospholamban and other regulatory proteins are considered important targets for drug development. In our experience, ischaemic preconditioning (IP) and pharmacological therapies, such as anti-oxidants, beta-adrenergic receptor blockers, angiotensin receptor (AT-1) blockers, angiotensin converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers are effective therapies that improve cardiac performance in the failing heart by improving SR function. Accordingly, this paper is intended to shed light on the knowledge in the field of cardiac therapy targeted to improve and protect SR function.
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Dhalla et al. (2001) studied this question.
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