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Article ; Online: So Many Targets.

Movsesian, Matthew

Journal of the American College of Cardiology

2017 Volume 69, Issue 4, Page(s) 434–436

MeSH term(s)	Calcium ; Disease Progression ; Heart Failure ; Humans ; Nod1 Signaling Adaptor Protein
Chemical Substances	NOD1 protein, human ; Nod1 Signaling Adaptor Protein ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2017-01-26
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	605507-2
ISSN	1558-3597 ; 0735-1097
ISSN (online)	1558-3597
ISSN	0735-1097
DOI	10.1016/j.jacc.2016.10.072
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Zs.A 1846: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 196: Show issues

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Article ; Online: Novel approaches to targeting PDE3 in cardiovascular disease.

Movsesian, Matthew

Pharmacology & therapeutics

2016 Volume 163, Page(s) 74–81

Abstract: Inhibitors of PDE3, a family of dual-specificity cyclic nucleotide phosphodiesterases, are used clinically to increase cardiac contractility by raising intracellular cAMP content in cardiac myocytes and to reduce vascular resistance by increasing ... ...

Abstract	Inhibitors of PDE3, a family of dual-specificity cyclic nucleotide phosphodiesterases, are used clinically to increase cardiac contractility by raising intracellular cAMP content in cardiac myocytes and to reduce vascular resistance by increasing intracellular cGMP content in vascular smooth muscle myocytes. When used in the treatment of patients with heart failure, PDE3 inhibitors are effective in the acute setting but increase sudden cardiac death with long-term administration, possibly reflecting pro-apoptotic and pro-hypertrophic consequences of increased cAMP-mediated signaling in cardiac myocytes. cAMP-mediated signaling in cardiac myocytes is highly compartmentalized, and different phosphodiesterases, by controlling cAMP content in functionally discrete intracellular microcompartments, regulate different cAMP-mediated pathways. Four variants/isoforms of PDE3 (PDE3A1, PDE3A2, PDE3A3, and PDE3B) are expressed in cardiac myocytes, and new experimental results have demonstrated that these isoforms, which are differentially localized intracellularly through unique protein-protein interactions, control different physiologic responses. While the catalytic regions of these isoforms may be too similar to allow the catalytic activity of each isoform to be selectively inhibited, targeting their unique protein-protein interactions may allow desired responses to be elicited without the adverse consequences that limit the usefulness of existing PDE3 inhibitors.
MeSH term(s)	Animals ; Cyclic AMP/biosynthesis ; Cyclic GMP/biosynthesis ; Cyclic Nucleotide Phosphodiesterases, Type 3/drug effects ; Cyclic Nucleotide Phosphodiesterases, Type 3/metabolism ; Heart Failure/drug therapy ; Heart Failure/mortality ; Heart Failure/physiopathology ; Humans ; Myocardial Contraction/physiology ; Myocytes, Cardiac/metabolism ; Myocytes, Smooth Muscle/metabolism ; Phosphodiesterase 3 Inhibitors/pharmacology ; Phosphorylation/physiology ; Protein Isoforms ; Signal Transduction/physiology
Chemical Substances	Phosphodiesterase 3 Inhibitors ; Protein Isoforms ; Cyclic AMP (E0399OZS9N) ; Cyclic Nucleotide Phosphodiesterases, Type 3 (EC 3.1.4.17) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2016-07
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2016.03.014
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Zs.A 1183: Show issues

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Article ; Online: New pharmacologic interventions to increase cardiac contractility: challenges and opportunities.

Movsesian, Matthew

Current opinion in cardiology

2015 Volume 30, Issue 3, Page(s) 285–291

Abstract: Purpose of review: The most extensively studied inotropic agents in patients with heart failure are phosphodiesterase (PDE) 3 inhibitors, which increase contractility by raising intracellular cyclic adenosine monophosphate content. In clinical trials, ... ...

Abstract	Purpose of review: The most extensively studied inotropic agents in patients with heart failure are phosphodiesterase (PDE) 3 inhibitors, which increase contractility by raising intracellular cyclic adenosine monophosphate content. In clinical trials, the inotropic benefits of these agents have been outweighed by an increase in sudden cardiac death. Here, I review recent findings that help explain what are likely to be distinct mechanisms involved in the beneficial and adverse effects of PDE3 inhibition. Recent findings: The proapoptotic consequences of PDE3 inhibition are becoming more apparent. Moreover, it has also become clear that individual PDE3 isoforms in cardiac myocytes are selectively regulated to interact with different proteins in different intracellular compartments. The beneficial and adverse effects of PDE3 inhibition may thus be attributable to the inhibition of different isoforms in different intracellular domains. In particular, PDE3A1 has been shown to interact directly with sarcoplasmic/endoplasmic reticulum Ca ATPase (SERCA2) in the sarcoplasmic reticulum through a phosphorylation of a site in its unique N-terminal domain, making it possible that this isoform can be selectively targeted to increase intracellular Ca cycling. Summary: Conventional PDE3 inhibitors target several functionally distinct isoforms of these enzymes. Isoform-selective and/or compartment-selective targeting of PDE3, through its protein-protein interactions, may produce the inotropic benefits of PDE3 inhibition without the adverse consequences.
MeSH term(s)	Age Factors ; Cardiomyopathy, Dilated/drug therapy ; Cardiotonic Agents/adverse effects ; Cardiotonic Agents/therapeutic use ; Cyclic AMP/metabolism ; Death, Sudden, Cardiac/etiology ; Heart Failure/drug therapy ; Humans ; Myocardial Contraction ; Myocytes, Cardiac/metabolism ; Phosphodiesterase 3 Inhibitors/adverse effects ; Phosphodiesterase 3 Inhibitors/therapeutic use ; Signal Transduction
Chemical Substances	Cardiotonic Agents ; Phosphodiesterase 3 Inhibitors ; Cyclic AMP (E0399OZS9N)
Language	English
Publishing date	2015-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	645186-x
ISSN	1531-7080 ; 0268-4705
ISSN (online)	1531-7080
ISSN	0268-4705
DOI	10.1097/HCO.0000000000000165
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Zs.A 2556: Show issues

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Article: The academic paradigm is the problem.

Movsesian, Matthew A

Journal of investigative medicine : the official publication of the American Federation for Clinical Research

2009 Volume 57, Issue 5, Page(s) 632–633

MeSH term(s)	Biomedical Research/methods ; Cooperative Behavior ; Heart Failure/drug therapy ; Humans ; United States
Language	English
Publishing date	2009-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1217870-6
ISSN	1708-8267 ; 1081-5589 ; 0009-9279
ISSN (online)	1708-8267
ISSN	1081-5589 ; 0009-9279
DOI	10.2310/JIM.0b013e3181a0a24e
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Zs.A 307: Show issues

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Article ; Online: Intramural conflicts of interest warrant scrutiny, too.

Movsesian, Matthew

Nature medicine

2011 Volume 17, Issue 5, Page(s) 534

MeSH term(s)	Conflict of Interest/economics ; Faculty, Medical ; Humans ; Physician Incentive Plans ; Schools, Medical/economics ; Schools, Medical/ethics ; United States
Language	English
Publishing date	2011-05-05
Publishing country	United States
Document type	News
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/nm0511-534
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Zs.A 4212: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 39: Show issues

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Article: Phosphodiesterase inhibition in heart failure.

Movsesian, Matthew A / Kukreja, Rakesh C

Handbook of experimental pharmacology

2011 , Issue 204, Page(s) 237–249

Abstract: Compounds that inhibit the catalytic activity of cyclic nucleotide phosphodiesterases are used as therapeutic agents to increase intracellular cAMP and/or cGMP content in cells or tissues of interest. In patients with heart failure, inhibitors of enzymes ...

Abstract	Compounds that inhibit the catalytic activity of cyclic nucleotide phosphodiesterases are used as therapeutic agents to increase intracellular cAMP and/or cGMP content in cells or tissues of interest. In patients with heart failure, inhibitors of enzymes in the PDE3 family of cyclic nucleotide phosphodiesterases are used to raise intracellular cAMP content in cardiac muscle, with inotropic actions. These drugs are effective in acute applications, but their long-term use has been complicated by an increase in cardiovascular mortality in clinical trials. Inhibitors of enzymes in the PDE5 family have been used to raise cGMP content in cardiac muscle in animal models of pressure overload, chronic β-adrenergic receptor stimulation, ischemic injury, and doxorubicin toxicity, and have been shown to have antihypertrophic and cardioprotective actions. Recent experimental results raise some question as to the likely applicability of these findings to humans, in whose hearts PDE5 is present at much lower levels than those seen in animal models, and raise the possibility of PDE1, a dual-specificity phosphodiesterase present at high levels in human myocardium, as an alternative target for inotropic and cardioprotective actions.
MeSH term(s)	Animals ; Cyclic AMP/analysis ; Cyclic GMP/analysis ; Heart Failure/drug therapy ; Heart Failure/enzymology ; Humans ; Phosphodiesterase 3 Inhibitors/therapeutic use ; Phosphodiesterase 4 Inhibitors/therapeutic use ; Phosphodiesterase 5 Inhibitors/therapeutic use ; Phosphodiesterase Inhibitors/therapeutic use
Chemical Substances	Phosphodiesterase 3 Inhibitors ; Phosphodiesterase 4 Inhibitors ; Phosphodiesterase 5 Inhibitors ; Phosphodiesterase Inhibitors ; Cyclic AMP (E0399OZS9N) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2011
Publishing country	Germany
Document type	Journal Article ; Review
ISSN	0171-2004
ISSN	0171-2004
DOI	10.1007/978-3-642-17969-3_10
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Sign. bis Bd. 125 (1997): 1982 A 2146: Show issues
danach: Sign. bei den Einzelbänden: Show issues

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Article: Altered cAMP-mediated signalling and its role in the pathogenesis of dilated cardiomyopathy.

Movsesian, Matthew A

Cardiovascular research

2004 Volume 62, Issue 3, Page(s) 450–459

Abstract: Alterations in the level and function of proteins involved in cAMP-mediated signalling are important in the pathophysiology and treatment of dilated cardiomyopathy. What is unclear is the extent to which these alterations, which attenuate receptor- ... ...

Abstract	Alterations in the level and function of proteins involved in cAMP-mediated signalling are important in the pathophysiology and treatment of dilated cardiomyopathy. What is unclear is the extent to which these alterations, which attenuate receptor-stimulated cAMP generation, contribute to the pathogenesis of dilated cardiomyopathy and the extent to which they constitute a beneficial compensatory response. Studies in animals involving overexpression and ablation of proteins or peptides involved in cAMP-mediated signalling have yielded disparate results that are difficult to reconcile with a simple hypothesis. Our ability to understand these differences is limited by the lack of information on how these different genetic manipulations affect the phosphorylation of individual substrates of protein kinase A (PK-A) through which cAMP signals are transduced. This is important in view of evidence that the phosphorylation of individual PK-A substrates can be regulated selectively in different intracellular compartments, and that the phosphorylation of some PK-A substrates is increased in dilated cardiomyopathy while the phosphorylation of others is reduced. Approaches that quantify changes in the phosphorylation of individual PK-A substrates in models of dilated cardiomyopathy will provide information that may allow a better understanding of the pathogenesis of the syndrome and a more rational approach to its treatment.
MeSH term(s)	Animals ; Cardiomyopathy, Dilated/etiology ; Cardiomyopathy, Dilated/metabolism ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/genetics ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Humans ; Mice ; Mice, Transgenic ; Models, Animal ; Phosphorylation ; Receptors, Adrenergic, beta/metabolism ; Signal Transduction/physiology
Chemical Substances	Receptors, Adrenergic, beta ; Cyclic AMP (E0399OZS9N) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
Language	English
Publishing date	2004-06-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1016/j.cardiores.2004.01.035
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Zs.A 565: Show issues

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Article ; Online: Functions of PDE3 Isoforms in Cardiac Muscle.

Movsesian, Matthew / Ahmad, Faiyaz / Hirsch, Emilio

Journal of cardiovascular development and disease

2018 Volume 5, Issue 1

Abstract: Isoforms in the PDE3 family of cyclic nucleotide phosphodiesterases have important roles in cyclic nucleotide-mediated signalling in cardiac myocytes. These enzymes are targeted by inhibitors used to increase contractility in patients with heart failure, ...

Abstract	Isoforms in the PDE3 family of cyclic nucleotide phosphodiesterases have important roles in cyclic nucleotide-mediated signalling in cardiac myocytes. These enzymes are targeted by inhibitors used to increase contractility in patients with heart failure, with a combination of beneficial and adverse effects on clinical outcomes. This review covers relevant aspects of the molecular biology of the isoforms that have been identified in cardiac myocytes; the roles of these enzymes in modulating cAMP-mediated signalling and the processes mediated thereby; and the potential for targeting these enzymes to improve the profile of clinical responses.
Language	English
Publishing date	2018-02-06
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2777082-5
ISSN	2308-3425 ; 2308-3425
ISSN (online)	2308-3425
ISSN	2308-3425
DOI	10.3390/jcdd5010010
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Article: PDE3 inhibition in dilated cardiomyopathy: reasons to reconsider.

Movsesian, Matthew A

Journal of cardiac failure

2002 Volume 9, Issue 6, Page(s) 475–480

Abstract: Background: PDE3 cyclic nucleotide phosphodiesterases have important roles in regulating cAMP- and cGMP-mediated signaling. Drugs that inhibit these enzymes raise cAMP and cGMP content in cardiac and vascular smooth muscle and increase the ... ...

Abstract	Background: PDE3 cyclic nucleotide phosphodiesterases have important roles in regulating cAMP- and cGMP-mediated signaling. Drugs that inhibit these enzymes raise cAMP and cGMP content in cardiac and vascular smooth muscle and increase the phosphorylation of proteins by cAMP- and cGMP-dependent protein kinases (PK-A and PK-G), thereby eliciting inotropic and vasodilatory responses. Methods: Although these actions are beneficial acutely in patients with dilated cardiomyopathy, long-term use of these agents was shown in several clinical trials to increase mortality. Several new clinical studies, however, suggest PDE3 inhibitors may be safe and effective when used in conjunction with beta-adrenergic receptor antagonists, whereas new studies at the cellular and molecular levels indicate that there are several isoforms of these enzymes in cardiac and vascular myocytes that are likely to regulate cAMP content in different intracellular compartments. Conclusions: Both sets of observations suggest that PDE3 inhibition may be refined to allow more selective effects on phosphorylation of PK-A substrates, possibly allowing the beneficial effects of PDE3 inhibition to be separated from the adverse long-term consequences of their use.
MeSH term(s)	3',5'-Cyclic-AMP Phosphodiesterases/antagonists & inhibitors ; 3',5'-Cyclic-AMP Phosphodiesterases/metabolism ; Adrenergic beta-Antagonists/therapeutic use ; Cardiomyopathy, Dilated/drug therapy ; Cardiomyopathy, Dilated/metabolism ; Cardiomyopathy, Dilated/physiopathology ; Cyclic Nucleotide Phosphodiesterases, Type 3 ; Humans ; Myocardial Contraction/drug effects ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; Phosphodiesterase Inhibitors/therapeutic use ; Vasodilation/drug effects
Chemical Substances	Adrenergic beta-Antagonists ; Phosphodiesterase Inhibitors ; 3',5'-Cyclic-AMP Phosphodiesterases (EC 3.1.4.17) ; Cyclic Nucleotide Phosphodiesterases, Type 3 (EC 3.1.4.17)
Language	English
Publishing date	2002-10-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1281194-4
ISSN	1532-8414 ; 1071-9164
ISSN (online)	1532-8414
ISSN	1071-9164
DOI	10.1016/s1071-9164(03)00135-0
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Zs.A 4340: Show issues

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Article: PDE3 cyclic nucleotide phosphodiesterases and the compartmentation of cyclic nucleotide-mediated signalling in cardiac myocytes.

Movsesian, Matthew A

Basic research in cardiology

2002 Volume 97 Suppl 1, Page(s) I83–90

Abstract: PDE3 cyclic nucleotide phosphodiesterase inhibitors raise cAMP and cGMP content in cardiac and vascular myocytes. Their administration to patients with dilated cardiomyopathy leads to improvements in hemodynamic parameters in the short term but reduces ... ...

Abstract	PDE3 cyclic nucleotide phosphodiesterase inhibitors raise cAMP and cGMP content in cardiac and vascular myocytes. Their administration to patients with dilated cardiomyopathy leads to improvements in hemodynamic parameters in the short term but reduces survival with chronic administration. The reasons for this 'biphasic' response have not been elucidated, but it is likely that beneficial and harmful effects of PDE3 inhibition reflect the phosphorylation of different substrates of cAMP- and cGMP-dependent protein kinases (PK-A and PK-G). It is now apparent that cardiac and vascular myocytes contain several isoforms of PDE3 that differ in their intracellular distribution and thus regulate cAMP and cGMP levels in different subcellular compartments. These isoforms also differ in their regulation by extracellular signals that may be important in the pathophysiology of dilated cardiomyopathy. An intriguing possibility is that the beneficial and harmful effects of PDE3 inhibition may be attributable to the inhibition of different isoforms of these enzymes.
MeSH term(s)	3',5'-Cyclic-AMP Phosphodiesterases/genetics ; 3',5'-Cyclic-AMP Phosphodiesterases/physiology ; Animals ; Cyclic Nucleotide Phosphodiesterases, Type 3 ; Humans ; Isoenzymes/metabolism ; Molecular Biology ; Myocytes, Cardiac/physiology ; Nucleotides, Cyclic/physiology ; Signal Transduction/physiology
Chemical Substances	Isoenzymes ; Nucleotides, Cyclic ; 3',5'-Cyclic-AMP Phosphodiesterases (EC 3.1.4.17) ; Cyclic Nucleotide Phosphodiesterases, Type 3 (EC 3.1.4.17)
Language	English
Publishing date	2002-12-10
Publishing country	Germany
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	189755-x
ISSN	1435-1803 ; 0300-8428 ; 0175-9418
ISSN (online)	1435-1803
ISSN	0300-8428 ; 0175-9418
DOI	10.1007/s003950200035
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