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Editorial
. 2012 Sep 28;111(8):954-6.
doi: 10.1161/CIRCRESAHA.112.278416.

Nitroxyl, redox switches, cardiac myofilaments, and heart failure: a prequel to novel therapeutics?

Ying Ge, Richard L Moss
Editorial

Nitroxyl, redox switches, cardiac myofilaments, and heart failure: a prequel to novel therapeutics?

Ying Ge et al. Circ Res. .
No abstract available

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Figures

Figure 1
Figure 1. Schematic representation of HNO-induced disulfide effects on cardiac myofilaments
A. Chemical reactions showing (1) the release of HNO from NCA by hydrolysis; (2) reaction of HNO with thiols on cysteine forming N-hydroxysulfenamide intermediates, which leads to sulfinamide or disulfide formation in the presence of an additional free thiol. B. Schematic drawing showing that disulfide bond formation between key cysteines in actin and tropomyosin and in MLC1 and MHC increases maximum force and Ca2+ sensitivity. Modified with permission from Moss et al and Gao et al.
See this image and copyright information in PMC

Comment on

References

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MeSH terms