Literature DB >> 19127140

Novel therapies for cyclic GMP control of vascular smooth muscle growth.

David A Tulis1.   

Abstract

Cyclic GMP, guanosine 3',5'-cyclic monophosphate, is a critical and multifunctional second-messenger molecule that mediates diverse physiological and pathophysiological functions in cardiac and vascular tissues. Synthesized through nitric oxide, carbon monoxide, and/or natriuretic peptide-mediated guanylate cyclase stimulation and guanosine triphosphate dephosphorylation, cyclic GMP is capable of stimulating a cascade of serine/threonine kinase events, including signaling through cyclic GMP- and/or cyclic AMP-dependent protein kinases, eliciting protein kinase-independent actions such as modulation of ion channels or transporters, or undergoing hydrolytic degradation through actions of cyclic GMP-regulated phosphodiesterases. Substrates, enzymes, cofactors, and associated variables in this multifaceted system have historically been targets of vital pharmacotherapies with perhaps most common the use of vascular smooth muscle-targeting organonitrates in cardiac patients and phosphodiesterase inhibitors in individuals with erectile dysfunction. Accumulating basic science and clinical evidence, however, suggests that cyclic GMP signaling is compromised under conditions of disease or elevated physiological stresses. Moreover, nitric oxide can stimulate an array of cytotoxic effects and nitric oxide-based therapies can be limited by diminished bioactivity and the development of tachyphylaxis or tolerance after prolonged use. Consequently, an emerging area for clinical drug development and therapeutic drug evaluation for conditions of cardiovascular adversity has focused on identification of cyclic GMP signaling pathways that act under oxidized or nitric oxide-unresponsive conditions and/or that operate irrespective of nitric oxide-induced complications. The aim of this therapeutic review is to describe novel, nitric oxide-alternate avenues for cyclic GMP signaling in vascular smooth muscle growth with particular emphasis on pharmacotherapeutics of recently characterized cyclic GMP-specific approaches.

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Year:  2008        PMID: 19127140      PMCID: PMC2677189          DOI: 10.1097/MJT.0b013e318140052f

Source DB:  PubMed          Journal:  Am J Ther        ISSN: 1075-2765            Impact factor:   2.688


  63 in total

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2.  Inhibition of deactivation of NO-sensitive guanylyl cyclase accounts for the sensitizing effect of YC-1.

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Journal:  J Biol Chem       Date:  2002-04-26       Impact factor: 5.157

3.  Therapy with nitrates: increasing evidence of vascular toxicity.

Authors:  John D Parker
Journal:  J Am Coll Cardiol       Date:  2003-11-19       Impact factor: 24.094

4.  Effects of the sGC stimulator BAY 41-2272 are not mediated by phosphodiesterase 5 inhibition.

Authors:  Erwin Bischoff; Johannes-Peter Stasch
Journal:  Circulation       Date:  2004-09-21       Impact factor: 29.690

5.  Matrix metalloproteinase-9 overexpression enhances vascular smooth muscle cell migration and alters remodeling in the injured rat carotid artery.

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6.  Sensitizing soluble guanylyl cyclase to become a highly CO-sensitive enzyme.

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7.  Carbon monoxide suppresses arteriosclerotic lesions associated with chronic graft rejection and with balloon injury.

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Journal:  Nat Med       Date:  2003-01-21       Impact factor: 53.440

Review 8.  Salutary properties of YC-1 in the cardiovascular and hematological systems.

Authors:  David Anthony Tulis
Journal:  Curr Med Chem Cardiovasc Hematol Agents       Date:  2004-10

9.  YC-1 inhibited human platelet aggregation through NO-independent activation of soluble guanylate cyclase.

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Journal:  Br J Pharmacol       Date:  1995-10       Impact factor: 8.739

10.  Endothelium-derived relaxing factor from pulmonary artery and vein possesses pharmacologic and chemical properties identical to those of nitric oxide radical.

Authors:  L J Ignarro; R E Byrns; G M Buga; K S Wood
Journal:  Circ Res       Date:  1987-12       Impact factor: 17.367

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  10 in total

1.  Soluble guanylyl cyclase-activated cyclic GMP-dependent protein kinase inhibits arterial smooth muscle cell migration independent of VASP-serine 239 phosphorylation.

Authors:  Andrew W Holt; Danielle N Martin; Patti R Shaver; Shaquria P Adderley; Joshua D Stone; Chintamani N Joshi; Jake T Francisco; Robert M Lust; Douglas A Weidner; Brian M Shewchuk; David A Tulis
Journal:  Cell Signal       Date:  2016-06-11       Impact factor: 4.315

Review 2.  Novel protein kinase targets in vascular smooth muscle therapeutics.

Authors:  David A Tulis
Journal:  Curr Opin Pharmacol       Date:  2017-04-04       Impact factor: 5.547

3.  Antigrowth properties of BAY 41-2272 in vascular smooth muscle cells.

Authors:  Natalia N Mendelev; Verietta S Williams; David A Tulis
Journal:  J Cardiovasc Pharmacol       Date:  2009-02       Impact factor: 3.105

4.  The cyclic GMP modulators YC-1 and zaprinast reduce vessel remodeling through antiproliferative and proapoptotic effects.

Authors:  Amit N Keswani; Kelly J Peyton; William Durante; Andrew I Schafer; David A Tulis
Journal:  J Cardiovasc Pharmacol Ther       Date:  2009-04-02       Impact factor: 2.457

5.  The dopamine D3 receptor knockout mouse mimics aging-related changes in autonomic function and cardiac fibrosis.

Authors:  Tracy L Johnson; David A Tulis; Benjamin E Keeler; Jitka A Virag; Robert M Lust; Stefan Clemens
Journal:  PLoS One       Date:  2013-08-30       Impact factor: 3.240

6.  Phosphodiesterases Regulate BAY 41-2272-Induced VASP Phosphorylation in Vascular Smooth Muscle Cells.

Authors:  Shaquria P Adderley; Chintamani N Joshi; Danielle N Martin; David Anthony Tulis
Journal:  Front Pharmacol       Date:  2012-02-07       Impact factor: 5.810

Review 7.  Cyclic Nucleotide-Directed Protein Kinases in Cardiovascular Inflammation and Growth.

Authors:  Nathan A Holland; Jake T Francisco; Sean C Johnson; Joshua S Morgan; Troy J Dennis; Nishitha R Gadireddy; David A Tulis
Journal:  J Cardiovasc Dev Dis       Date:  2018-01-23

8.  Inhibition of vascular smooth muscle growth via signaling crosstalk between AMP-activated protein kinase and cAMP-dependent protein kinase.

Authors:  Joshua D Stone; Avinash Narine; David A Tulis
Journal:  Front Physiol       Date:  2012-10-29       Impact factor: 4.566

Review 9.  Adrenoreceptors and nitric oxide in the cardiovascular system.

Authors:  Valeria Conti; Giusy Russomanno; Graziamaria Corbi; Viviana Izzo; Carmine Vecchione; Amelia Filippelli
Journal:  Front Physiol       Date:  2013-11-06       Impact factor: 4.566

Review 10.  PDE-Mediated Cyclic Nucleotide Compartmentation in Vascular Smooth Muscle Cells: From Basic to a Clinical Perspective.

Authors:  Margarida Lorigo; Nelson Oliveira; Elisa Cairrao
Journal:  J Cardiovasc Dev Dis       Date:  2021-12-22
  10 in total

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