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. 2017:967:227-240.
doi: 10.1007/978-3-319-63245-2_13.

Redox Mechanisms Influencing cGMP Signaling in Pulmonary Vascular Physiology and Pathophysiology

Dhara Patel  1 , Anand Lakhkar  1 , Michael S Wolin  2
Affiliations

Redox Mechanisms Influencing cGMP Signaling in Pulmonary Vascular Physiology and Pathophysiology

Dhara Patel et al. Adv Exp Med Biol. 2017.

Abstract

The soluble form of guanylate cyclase (sGC) and cGMP signaling are major regulators of pulmonary vasodilation and vascular remodeling that protect the pulmonary circulation from hypertension development. Nitric oxide, reactive oxygen species, thiol and heme redox, and heme biosynthesis control mechanisms regulating the production of cGMP by sGC. In addition, a cGMP-independent mechanism regulates protein kinase G through thiol oxidation in manner controlled by peroxide metabolism and NADPH redox. Multiple aspects of these regulatory processes contribute to physiological and pathophysiological regulation of the pulmonary circulation, and create potentially novel therapeutic targets for the treatment of pulmonary vascular disease.

Keywords: Cyclic guanosine monophosphate; Heme redox; NADPH oxidase; Nitric oxide; Protein kinase G; Pulmonary vascular disease; Reactive oxygen species; Soluble guanylate cyclase; Thiol oxidation.

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Figures

Fig. 1
Fig. 1
cGMP-related signaling mechanisms regulating pulmonary vascular relaxation and remodeling.
Fig. 2
Fig. 2
Nitric oxide, reactive oxygen species, thiol and heme redox, and heme biosynthesis control mechanisms that regulate the production of cGMP by sGC and/or a cGMP-independent mechanism regulating protein kinase G.
Fig. 3
Fig. 3
Therapeutic targeting of cGMP signaling for the treatment of pulmonary vascular disease.
See this image and copyright information in PMC

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