Key result
End-stage failing hearts exhibit ~2-fold greater actin and tropomyosin carbonylation linked to reduced LVEF.
Why the study?
Although reactive oxygen/nitrogen species accumulation may play a key role in contractile dysfunction, data regarding contractile protein targets in human HF are lacking.
Observational
Effect estimate: 2.14-fold increase (actin) and 2.31-fold increase (tropomyosin)
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Highlights potential for targeting myofilament carbonylation in HF; leaves open whether this improves LVEF or outcomes.
Canton et al. (2011) conducted an observational in End-stage heart failure. End-stage heart failure (NYHA class IV) vs. Nonfailing donor hearts was evaluated on Carbonylation of actin and tropomyosin, disulphide cross-bridge formation, and S-nitrosylation (2.14-fold increase (actin) and 2.31-fold increase (tropomyosin)). End-stage failing hearts exhibited 2.14-fold and 2.31-fold greater levels of actin and tropomyosin carbonylation compared with nonfailing donor hearts, which correlated with reduced LVEF.
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