Abstract
Nitric oxide (NO) signaling mediates many important physiological processes through the receptor soluble guanylate cyclase (sGC). Under disease conditions sGC heme can be oxidized resulting in NO insensitivity. Here, we show that the therapeutic compound cinaciguat (Cin) rescues dysfunctional sGC by direct displacement of the oxidized heme.
Copyright © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Benzoates / chemistry*
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Enzyme Activators / chemistry*
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Guanylate Cyclase / chemistry*
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Guanylate Cyclase / metabolism
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Heme / chemistry
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Heme / metabolism
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Kinetics
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Nitric Oxide / chemistry
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Oxidation-Reduction
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Rats
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Receptors, Cytoplasmic and Nuclear / chemistry*
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Receptors, Cytoplasmic and Nuclear / metabolism
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Signal Transduction
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Soluble Guanylyl Cyclase
Substances
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Benzoates
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Enzyme Activators
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Receptors, Cytoplasmic and Nuclear
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Nitric Oxide
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BAY 58-2667
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Heme
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Guanylate Cyclase
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Soluble Guanylyl Cyclase