Key result
Chemical cross-linking revealed that phospholamban binding interactions with the Ca2+ pump are largely unchanged in failing myocardium compared to normal human hearts.
Population
Sarcoplasmic reticulum (SR) vesicles prepared from normal and failed human hearts
Design
Preclinical
Authors
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Preserved phospholamban-SERCA2a inhibition in failing hearts warrants no therapy change; leaves open whether targeting this interaction improves outcomes.
Phospholamban binding interactions with SERCA2a are largely unchanged in failing human myocardium, indicating the inhibitory mechanism remains intact.
Akin et al. (2012) studied Heart failure. Chemical cross-linking and anti-PLB antibody 2D12 vs. Normal human hearts was evaluated on Protein binding interactions between native phospholamban (PLB) and SERCA2a. Chemical cross-linking revealed that phospholamban binding interactions with the Ca2+ pump are largely unchanged in failing myocardium compared to normal human hearts.
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