This review highlights the critical role of altered intracellular calcium handling and sarcoplasmic reticulum protein abnormalities in the progression of heart failure.
Defective SR Ca2+ handling may drive HF progression; leaves open whether targeting these proteins improves outcomes.
Structural and functional alterations in the Ca2+ regulatory proteins present in the sarcoplasmic reticulum have recently been shown to be strongly involved in the pathogenesis of heart failure. Chronic activation of the sympathetic nervous system or of the renin-angiotensin system induces abnormalities in both the function and structure of these proteins. We review here the considerable body of evidence that has accumulated to support the notion that such abnormalities contribute to a defectiveness of contractile performance and hence to the progression of heart failure.
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Yano et al. (2005) studied this question.
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