Key result
Suppression of O2 consumption for total Ca2+ handling, mainly utilized by SERCA2, is a major cause of failing hearts, mediated through degradation of membrane alpha-fodrin or suppressed SERCA2 expression.
Population
Cross-circulated excised rat heart preparations from models of acute and chronic failing hearts
Design
Review
Authors
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Supports mechanistic research on SERCA2 and alpha-fodrin in HF; leaves open clinical translation from rat models.
In failing rat hearts, impaired total Ca2+ handling due to SERCA2 suppression or calpain-mediated alpha-fodrin degradation leads to decreased oxygen consumption for excitation-contraction coupling.
Yoshikawa et al. (2004) conducted a review in Heart failure. Heart failure models (high Ca2+, ischemia-reperfusion, DM, hypothyroidism) vs. Normal rat hearts was evaluated on Myocardial O2 consumption per beat (VO2) and systolic pressure-volume area (PVA) relation, and SERCA2 protein levels. Suppression of O2 consumption for total Ca2+ handling, mainly utilized by SERCA2, is a major cause of failing hearts, mediated through degradation of membrane alpha-fodrin or suppressed SERCA2 expression.
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