Cyclic
            <scp>GMP</scp>
            Dependent Protein Kinase (
            <scp>c</scp>
            <scp>GK</scp>
            ,
            <scp>PKG</scp>
            )

Smolenski, Albert; Lohmann, Suzanne M.

doi:10.1002/0471203076.emm0423

Cited by 2 publications

(1 citation statement)

References 36 publications

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“…45 Insight into cGK functions has been obtained both from analyses of substrates phosphorylated by cGKs and from cGK knockout mice. cGKI substrates and functions (Table) have been reviewed 11,14,46,47 and are briefly discussed here. Except for CFTR, 48 there are almost no other well-studied substrates of cGKII.…”

Section: Cgmp-dependent Protein Kinasesmentioning

confidence: 99%

Physiology and Pathophysiology of Vascular Signaling Controlled by Cyclic Guanosine 3′,5′-Cyclic Monophosphate–Dependent Protein Kinase

et al. 2003

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D espite impressive medical advances 1 that have led to diminished cardiovascular death rates in some countries over the past 20 years, cardiovascular disease remains the leading cause of death in developed countries such as the United States. This promises to worsen as a result of aging populations; the incipient obesity and type II diabetes epidemic; sedentary lifestyle; and continued abuse of tobacco, alcohol, and other substances. Cardiovascular disease is clearly multifactorial, and the approach to its prevention necessarily likewise. Candidates for prevention include cyclic guanosine 3Ј,5Ј-cyclic monophosphate (cGMP)-dependent signaling networks initiated by natriuretic peptides (NPs) and nitric oxide (NO), which demonstrate characteristics deemed worthy of diagnostic and therapeutic exploitation. cGMP signaling contributes to the function and interaction of several vascular cell types, and its dysfunction could be involved in major destructive processes such as atherosclerosis, hypertension, diabetic complications, (re)stenosis, and tissue infarction, as well as the undermining of clinical therapy like in the case of nitrate tolerance. This review takes a focused look at key elements of the cGMP signaling cascade in vascular tissue, particularly recent advances in our knowledge of cGMP-dependent protein kinase (cGK, also known as PKG) function. Finally, we discuss the potential of clinical monitoring of cGK activity for assessing the functional status of cGMP signaling and for guiding the design of therapeutic strategies to improve vascular function. cGMP SynthesisOne of the 2 major synthetic pathways for cGMP generation from guanosine 5Ј-triphosphate (GTP) is directed by NPs (Figure 1), consisting of atrial (ANP), B-type (BNP), and C-type (CNP) natriuretic peptides, which act via the membrane receptor guanylate cyclases GC-A (highest affinity for ANP, BNP) and GC-B (highest affinity for CNP). ANP and BNP, released from the heart by mechanical stretch in response to increased atrial pressure/volume, and CNP, released from the endothelium, can all cause smooth muscle (SM) relaxation and vasodilation. 2,3 Particularly, ANP has multiple effects, which lead to vascular smooth muscle (VSM) relaxation, increased vascular permeability and glomerular filtration rate, inhibition of the sympathetic and renin-angiotensin-aldosterone systems, and natriuresis/diuresis. 3 Germline deletion of ANP or its GC-A receptor in mice resulted in varying degrees of hypertension, cardiomyopathy, and heart failure (reviewed in reference 2 ), but also cardiac hypertrophy that is independent of hypertension. 4,5 ANP effects on VSM itself were analyzed in transgenic mice engineered to lack GC-A selectively in smooth muscle. These mice displayed resistance to vasodilation by acute ANP treatment or vascular volume expansion, but normal resting blood pressure, 6 suggesting that the function of GC-A in VSM can be compensated for in chronic blood pressure regulation.The second major pathway for cGMP synthesis (Figure 1) entails stimulatio...

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Section: Cgmp-dependent Protein Kinasesmentioning

confidence: 99%

Physiology and Pathophysiology of Vascular Signaling Controlled by Cyclic Guanosine 3′,5′-Cyclic Monophosphate–Dependent Protein Kinase

et al. 2003

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Physiology and pathophysiology of vascular signaling controlled by guanosine 3',5'-cyclic monophosphate-dependent protein kinase.

Birschmann

Walter²

2004

Acta Biochim Pol

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Recent medical advances suggest that the cellular natriuretic peptide/cGMP and NO/cGMP effector systems represent important signal transduction pathways especially in the cardiovascular system. These pathways also appear to be very interesting targets for the possible prevention of cardiovascular diseases. Exciting candidates for prevention include cGMP-dependent signaling networks initiated by natriuretic peptides (NP) and nitric oxide (NO) which are currently explored for their diagnostic and therapeutic potential. cGMP signaling contributes to the function and interaction of several vascular cell types, and its dysfunction is involved in the progression of major cardiovascular diseases such as atherosclerosis, hypertension and diabetic complications. This review will take a focussed look at key elements of the cGMP signaling cascade in vascular tissue. Recent advances in our knowledge of cGMP-dependent protein kinases (cGK, also known as PKG), the potential for assessing the functional status of cGMP signaling and the possible cross talk with insulin signaling will be reviewed.

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Cyclic GMP Dependent Protein Kinase ( c GK , PKG )

Cited by 2 publications

References 36 publications

Physiology and Pathophysiology of Vascular Signaling Controlled by Cyclic Guanosine 3′,5′-Cyclic Monophosphate–Dependent Protein Kinase

Physiology and Pathophysiology of Vascular Signaling Controlled by Cyclic Guanosine 3′,5′-Cyclic Monophosphate–Dependent Protein Kinase

Physiology and pathophysiology of vascular signaling controlled by guanosine 3',5'-cyclic monophosphate-dependent protein kinase.

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