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Article ; Online: The Complexity and Multiplicity of the Specific cAMP Phosphodiesterase Family: PDE4, Open New Adapted Therapeutic Approaches.

Lugnier, Claire

International journal of molecular sciences

2022 Volume 23, Issue 18

Abstract: Cyclic nucleotides (cAMP, cGMP) play a major role in normal and pathologic signaling. Beyond receptors, cyclic nucleotide phosphodiesterases; (PDEs) rapidly convert the cyclic nucleotide in its respective 5'-nucleotide to control intracellular cAMP and/ ... ...

Abstract	Cyclic nucleotides (cAMP, cGMP) play a major role in normal and pathologic signaling. Beyond receptors, cyclic nucleotide phosphodiesterases; (PDEs) rapidly convert the cyclic nucleotide in its respective 5'-nucleotide to control intracellular cAMP and/or cGMP levels to maintain a normal physiological state. However, in many pathologies, dysregulations of various PDEs (PDE1-PDE11) contribute mainly to organs and tissue failures related to uncontrolled phosphorylation cascade. Among these, PDE4 represents the greatest family, since it is constituted by 4 genes with multiple variants differently distributed at tissue, cellular and subcellular levels, allowing different fine-tuned regulations. Since the 1980s, pharmaceutical companies have developed PDE4 inhibitors (PDE4-I) to overcome cardiovascular diseases. Since, they have encountered many undesired problems, (emesis), they focused their research on other PDEs. Today, increases in the knowledge of complex PDE4 regulations in various tissues and pathologies, and the evolution in drug design, resulted in a renewal of PDE4-I development. The present review describes the recent PDE4-I development targeting cardiovascular diseases, obesity, diabetes, ulcerative colitis, and Crohn's disease, malignancies, fatty liver disease, osteoporosis, depression, as well as COVID-19. Today, the direct therapeutic approach of PDE4 is extended by developing allosteric inhibitors and protein/protein interactions allowing to act on the PDE interactome.
MeSH term(s)	3',5'-Cyclic-AMP Phosphodiesterases ; COVID-19 ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/genetics ; Cyclic GMP ; Cyclic Nucleotide Phosphodiesterases, Type 4 ; Diethylstilbestrol/analogs & derivatives ; Humans ; Nucleotides, Cyclic ; Pharmaceutical Preparations ; Phosphodiesterase 4 Inhibitors ; Phosphoric Diester Hydrolases
Chemical Substances	Nucleotides, Cyclic ; Pharmaceutical Preparations ; Phosphodiesterase 4 Inhibitors ; diethylstilbestrol monophosphate (47341-71-9) ; Diethylstilbestrol (731DCA35BT) ; Phosphoric Diester Hydrolases (EC 3.1.4.-) ; 3',5'-Cyclic-AMP Phosphodiesterases (EC 3.1.4.17) ; Cyclic Nucleotide Phosphodiesterases, Type 4 (EC 3.1.4.17) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2022-09-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms231810616
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Book: Phosphodiesterase

Lugnier, Claire

methods and protocols

(Methods in molecular biology ; 307)

2005

Author's details	ed. by Claire Lugnier
Series title	Methods in molecular biology ; 307
Collection
Keywords	Phosphoric Diester Hydrolases / physiology ; Phosphoric Diester Hydrolases / analysis ; Protein Engineering / methods ; Biological Assay / methods ; Phosphodiesterasen ; Labortechnik ; Bioassay
Subject	Biologische Prüfung ; EC 3.1.4 ; Phosphorsäurediesterasen ; Laboratorium ; Laboratoriumstechnik ; Labormethode
Language	English
Size	XII, 324 S. : Ill., graph. Darst.
Publisher	Humana Press
Publishing place	Totowa, NJ
Publishing country	United States
Document type	Book
Note	Includes bibliographical references and index
HBZ-ID	HT014503498
ISBN	1-58829-314-9 ; 978-1-58829-314-5
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Article ; Online: PDE4 inhibition as a therapeutic strategy for improvement of pulmonary dysfunctions in Covid-19 and cigarette smoking.

Lugnier, Claire / Al-Kuraishy, Hayder M / Rousseau, Eric

Biochemical pharmacology

2021 Volume 185, Page(s) 114431

Abstract: Angiotensin-converting enzyme 2 (ACE2) is the binding-site and entry-point for SARS-CoV-2 in human and highly expressed in the lung. Cigarette smoking (CS) is the leading cause of pulmonary and cardiovascular diseases. Chronic CS leads to upregulation of ...

Abstract	Angiotensin-converting enzyme 2 (ACE2) is the binding-site and entry-point for SARS-CoV-2 in human and highly expressed in the lung. Cigarette smoking (CS) is the leading cause of pulmonary and cardiovascular diseases. Chronic CS leads to upregulation of bronchial ACE2 inducing a high vulnerability in COVID-19 smoker patients. Interestingly, CS-induced dysregulation of pulmonary renin-angiotensin system (RAS) in part contributing into the potential pathogenesis COVID-19 pneumonia and acute respiratory distress syndrome (ARDS). Since, CS-mediated ACE2 activations is not the main pathway for increasing the risk of COVID-19, it appeared that AngII/AT
MeSH term(s)	Angiotensin-Converting Enzyme Inhibitors/pharmacology ; Angiotensin-Converting Enzyme Inhibitors/therapeutic use ; Animals ; COVID-19/drug therapy ; COVID-19/epidemiology ; COVID-19/metabolism ; Cigarette Smoking/drug therapy ; Cigarette Smoking/epidemiology ; Cigarette Smoking/metabolism ; Humans ; Lung/drug effects ; Lung/physiology ; Lung Diseases/drug therapy ; Lung Diseases/epidemiology ; Lung Diseases/metabolism ; Peptidyl-Dipeptidase A/metabolism ; Phosphodiesterase 4 Inhibitors/pharmacology ; Phosphodiesterase 4 Inhibitors/therapeutic use ; Respiratory Distress Syndrome/drug therapy ; Respiratory Distress Syndrome/epidemiology ; Respiratory Distress Syndrome/metabolism
Chemical Substances	Angiotensin-Converting Enzyme Inhibitors ; Phosphodiesterase 4 Inhibitors ; Peptidyl-Dipeptidase A (EC 3.4.15.1)
Language	English
Publishing date	2021-01-28
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2021.114431
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Article ; Online: Cyclic nucleotide phosphodiesterases: New targets in the metabolic syndrome?

Lugnier, Claire / Meyer, Alain / Talha, Samy / Geny, Bernard

Pharmacology & therapeutics

2020 Volume 208, Page(s) 107475

Abstract: Metabolic diseases have a tremendous impact on human morbidity and mortality. Numerous targets regulating adenosine monophosphate kinase (AMPK) have been identified for treating the metabolic syndrome (MetS), and many compounds are being used or ... ...

Abstract	Metabolic diseases have a tremendous impact on human morbidity and mortality. Numerous targets regulating adenosine monophosphate kinase (AMPK) have been identified for treating the metabolic syndrome (MetS), and many compounds are being used or developed to increase AMPK activity. In parallel, the cyclic nucleotide phosphodiesterase families (PDEs) have emerged as new therapeutic targets in cardiovascular diseases, as well as in non-resolved pathologies. Since some PDE subfamilies inactivate cAMP into 5'-AMP, while the beneficial effects in MetS are related to 5'-AMP-dependent activation of AMPK, an analysis of the various controversial relationships between PDEs and AMPK in MetS appears interesting. The present review will describe the various PDE families, AMPK and molecular mechanisms in the MetS and discuss the PDEs/PDE modulators related to the tissues involved, thus supporting the discovery of original molecules and the design of new therapeutic approaches in MetS.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Animals ; Humans ; Metabolic Syndrome/drug therapy ; Metabolic Syndrome/metabolism ; Nucleotides, Cyclic ; Phosphodiesterase Inhibitors/therapeutic use ; Phosphoric Diester Hydrolases/metabolism
Chemical Substances	Nucleotides, Cyclic ; Phosphodiesterase Inhibitors ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Phosphoric Diester Hydrolases (EC 3.1.4.-)
Language	English
Publishing date	2020-01-09
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.2020.107475
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Article ; Online: NCS 613, a PDE4 inhibitor, by increasing cAMP level suppresses systemic inflammation and immune complexes deposition in kidney of MRL/lpr lupus- prone mice.

Yougbare, Issaka / Keravis, Thérèse / Lugnier, Claire

Biochimica et biophysica acta. Molecular basis of disease

2020 Volume 1867, Issue 3, Page(s) 166019

Abstract: Nephritis remains the most common severe manifestation of systemic lupus erythematosus in which auto-antibodies mediate chronic inflammation and kidney damage. cAMP-phosphodiesterases regulate sodium excretion and inflammation in various tissues. How ... ...

Abstract	Nephritis remains the most common severe manifestation of systemic lupus erythematosus in which auto-antibodies mediate chronic inflammation and kidney damage. cAMP-phosphodiesterases regulate sodium excretion and inflammation in various tissues. How cAMP elevation can reduce systemic inflammation and suppress kidney inflammation and damage remains elusive. PDE4 signaling and cAMP metabolism were investigated along immune complex depositions in target tissues and kidney damage (histology). SLE disease progression is associated with changes in kidney PDE4 activity and expression. Moreover, lupus prone mice exhibit low kidney cAMP level which is associated to induction and relocation of nuclear and cytoskeleton PDE4 isoforms. Auto-antibodies-induced kidney damage was attested by mesangial proliferation and cellular infiltration. Interestingly, we reported that NCS 613 treatment decreases systemic auto-antibody secretion and their corresponding immune complex deposition in target tissues. Furthermore, NCS 613 is able to increase cAMP levels in the kidney; hence this compound rescues kidney PDE4 alterations in treated mice. NCS 613 overcomes disease progression in lupus prone mice by improving wellbeing and decreasing inflammation in treated mice. The PDE4 inhibitor, NCS 613, is a new anti-inflammatory compound that is believed to be a leading drug candidate for the treatment of inflammatory diseases such as lupus nephritis.
MeSH term(s)	Adenine/analogs & derivatives ; Adenine/pharmacology ; Adenine/therapeutic use ; Animals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Antigen-Antibody Complex/analysis ; Antigen-Antibody Complex/immunology ; Cyclic AMP/analysis ; Cyclic AMP/immunology ; Female ; Inflammation/drug therapy ; Inflammation/immunology ; Inflammation/pathology ; Kidney/drug effects ; Kidney/immunology ; Kidney/pathology ; Lupus Erythematosus, Systemic/drug therapy ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/pathology ; Lupus Nephritis/drug therapy ; Lupus Nephritis/immunology ; Lupus Nephritis/pathology ; Mice, Inbred MRL lpr ; Phosphodiesterase 4 Inhibitors/pharmacology ; Phosphodiesterase 4 Inhibitors/therapeutic use ; Mice
Chemical Substances	2-trifluoromethyl-9-(2-fluorophenylmethyl)-N-methyladenine ; Anti-Inflammatory Agents ; Antigen-Antibody Complex ; Phosphodiesterase 4 Inhibitors ; Cyclic AMP (E0399OZS9N) ; Adenine (JAC85A2161)
Language	English
Publishing date	2020-11-21
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2020.166019
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Article ; Online: PDE inhibitors: a new approach to treat metabolic syndrome?

Lugnier, Claire

Current opinion in pharmacology

2011 Volume 11, Issue 6, Page(s) 698–706

Abstract: About one third of people in the world suffer from metabolic syndrome (MetS), with symptoms such as hypertension and elevated blood cholesterol, and with increased risk of developing additional diseases such as diabetes mellitus and heart disease. The ... ...

Abstract	About one third of people in the world suffer from metabolic syndrome (MetS), with symptoms such as hypertension and elevated blood cholesterol, and with increased risk of developing additional diseases such as diabetes mellitus and heart disease. The progression of this multifactorial pathology, which targets various tissues and organs, might necessitate a renewal in therapeutic approaches. Since cyclic nucleotide phosphodiesterases (PDEs), enzymes which hydrolyze cyclic AMP and cyclic GMP, play a crucial role in regulating endocrine and cardiovascular functions, inflammation, oxidative stress, and cell proliferation, all of which contribute to MetS, we wonder whether PDE inhibitors might represent new therapeutic approaches for preventing and treating MetS.
MeSH term(s)	3',5'-Cyclic-AMP Phosphodiesterases/antagonists & inhibitors ; 3',5'-Cyclic-AMP Phosphodiesterases/metabolism ; 3',5'-Cyclic-GMP Phosphodiesterases/antagonists & inhibitors ; 3',5'-Cyclic-GMP Phosphodiesterases/metabolism ; Animals ; Cyclic AMP/antagonists & inhibitors ; Cyclic AMP/physiology ; Cyclic GMP/antagonists & inhibitors ; Cyclic GMP/physiology ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/enzymology ; Endothelium, Vascular/metabolism ; Heart/drug effects ; Humans ; Isoenzymes/antagonists & inhibitors ; Isoenzymes/metabolism ; Metabolic Syndrome/drug therapy ; Metabolic Syndrome/enzymology ; Metabolic Syndrome/metabolism ; Molecular Targeted Therapy ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/enzymology ; Muscle, Smooth, Vascular/metabolism ; Myocardium/enzymology ; Myocardium/metabolism ; Phosphodiesterase Inhibitors/pharmacology ; Phosphodiesterase Inhibitors/therapeutic use
Chemical Substances	Isoenzymes ; Phosphodiesterase Inhibitors ; Cyclic AMP (E0399OZS9N) ; 3',5'-Cyclic-AMP Phosphodiesterases (EC 3.1.4.17) ; 3',5'-Cyclic-GMP Phosphodiesterases (EC 3.1.4.35) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2011-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2011.09.012
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Article ; Online: Therapeutic potentials of natural compounds acting on cyclic nucleotide phosphodiesterase families.

Abusnina, Abdurazzag / Lugnier, Claire

Cellular signalling

2017 Volume 39, Page(s) 55–65

Abstract: Intracellular cyclic AMP and/or cyclic GMP are characterized in the 1960th. These second messengers, hydrolysed specifically by cyclic nucleotide phosphodiesterase (PDE), play a major role in intracellular signalling. Natural products have been a rich ... ...

Abstract	Intracellular cyclic AMP and/or cyclic GMP are characterized in the 1960th. These second messengers, hydrolysed specifically by cyclic nucleotide phosphodiesterase (PDE), play a major role in intracellular signalling. Natural products have been a rich source of drug discovery, Theophylline and Methylxanthine originated from tea leaves used for asthma treatment, whereas, Papaverine, a natural isoquinolein originated from Papaver somniferum traditionally used in impotency, altogether as caffeine where firstly described as PDE-inhibiting compounds. Since that time, the knowledge in PDE field has been drastically increased, allowing the design and development of new therapeutic drugs acting against different pathologies in the nanomolar range. During this period some natural compounds have been identified as PDE inhibitors and used in that context to investigate their therapeutic potential effects. The aim of this literature review is to point out the reported data and demonstrating the contribution of natural characterized molecules as PDE inhibitors in various pathologies that can open new fields of research for drug discovery, notably in epigenetic regulation.
MeSH term(s)	3',5'-Cyclic-AMP Phosphodiesterases/antagonists & inhibitors ; Animals ; Asthma/drug therapy ; Biological Products/pharmacology ; Biological Products/therapeutic use ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Drug Discovery ; Epigenesis, Genetic/drug effects ; Humans ; Inflammation/drug therapy ; Mice ; Neovascularization, Pathologic/drug therapy ; Papaverine/pharmacology ; Papaverine/therapeutic use ; Phosphodiesterase Inhibitors/pharmacology ; Phosphodiesterase Inhibitors/therapeutic use ; Theophylline/pharmacology ; Theophylline/therapeutic use ; Xanthines/pharmacology ; Xanthines/therapeutic use
Chemical Substances	Biological Products ; Phosphodiesterase Inhibitors ; Xanthines ; methylxanthine (28109-92-4) ; Theophylline (C137DTR5RG) ; Papaverine (DAA13NKG2Q) ; 3',5'-Cyclic-AMP Phosphodiesterases (EC 3.1.4.17)
Language	English
Publishing date	2017-07-25
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2017.07.018
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Article ; Online: Statins Therapy Improves Acute Ischemic Stroke in Patients with Cardio-metabolic Disorders Measured by Lipoprotein-Associated Phospholipase A2 (Lp-PLA2): New Focal Point.

Al-Kuraishy, Hayder M / Hussien, Nawar R / Al-Naimi, Marwa S / Al-Gareeb, Ali I / Lugnier, Claire

Neurology India

2022 Volume 69, Issue 6, Page(s) 1637–1644

Abstract: Background: Acute ischemic stroke (AIS) leads to neuronal and endothelial damage that activate the release of proinflammatory mediators such as lipoprotein-associated phospholipase A2 (Lp-PLA2), which lead to the development of brain edema injury. Most ... ...

Abstract	Background: Acute ischemic stroke (AIS) leads to neuronal and endothelial damage that activate the release of proinflammatory mediators such as lipoprotein-associated phospholipase A2 (Lp-PLA2), which lead to the development of brain edema injury. Most of statins produce differential effects on Lp-PLA2 activity and mass with a comparable reduction in low-density lipoprotein (LDL) serum levels. Aims: The aim of this study is to evaluate the differential effect of different statins on the mass of level of Lp-PLA2 in patients with AIS. Methods: A total of 69 patients with AIS aged 40-70 years compared with matched 39 healthy controls were involved in this case-control study. The AIS patients were divided according to the statins therapy into 39 patients on statins therapy (statins on), and 30 patients were not on the statins therapy (statins off). Anthropometric variables including weight, height, body mass index (BMI), and blood pressure profile were estimated. Besides, biochemical variables including lipid profile[total cholesterol (TC), triglyceride (TG), LDL, very low-density lipoprotein (VLDL), high-density lipoprotein (HDL)], Lp-PLA2 mass levels, high-sensitive C-reactive protein (Hs-CRP) were estimated. Results: Patients with AIS had high Lp-PLA2 mass levels (P < 0.01) that positively correlated with high Hs-CRP, blood pressure, BMI, TC, TG, VLDL, LDL, and negatively correlated with HDL as compared with healthy controls. As well, statins on patients had lower Lp-PLA2 mass levels (9.82 ± 3.19 IU/mL) compared with statins off patients (16.55 ± 4.72 IU/mL), (P = 0.0001). Regarding the gender differences in the Lp-PLA2 mass level, it was higher in men patients with AIS compared with comparable females (P = 0.03). Conclusions: Lp-PLA2 mass level was higher in patients with AIS and linked with underlying poor cardio-metabolic disorders. Therefore, the Lp-PLA2 mass level is observed to be a surrogate biomarker of AIS mainly in patients with poor cardio-metabolic disorders. Statin therapy improves the Lp-PLA2 mass level and the poor cardio-metabolic profile in patients with AIS.
MeSH term(s)	1-Alkyl-2-acetylglycerophosphocholine Esterase ; Biomarkers ; Brain Ischemia/drug therapy ; Case-Control Studies ; Female ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use ; Ischemic Stroke ; Male ; Metabolic Diseases ; Risk Factors ; Stroke/drug therapy
Chemical Substances	Biomarkers ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; 1-Alkyl-2-acetylglycerophosphocholine Esterase (EC 3.1.1.47)
Language	English
Publishing date	2022-01-01
Publishing country	India
Document type	Journal Article
ZDB-ID	415522-1
ISSN	1998-4022 ; 0028-3886
ISSN (online)	1998-4022
ISSN	0028-3886
DOI	10.4103/0028-3886.333482
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Article: PDE inhibitors: a new approach to treat metabolic syndrome?

Lugnier, Claire

Current opinion in pharmacology. 2011 Dec., v. 11, no. 6

2011

Abstract	About one third of people in the world suffer from metabolic syndrome (MetS), with symptoms such as hypertension and elevated blood cholesterol, and with increased risk of developing additional diseases such as diabetes mellitus and heart disease. The progression of this multifactorial pathology, which targets various tissues and organs, might necessitate a renewal in therapeutic approaches. Since cyclic nucleotide phosphodiesterases (PDEs), enzymes which hydrolyze cyclic AMP and cyclic GMP, play a crucial role in regulating endocrine and cardiovascular functions, inflammation, oxidative stress, and cell proliferation, all of which contribute to MetS, we wonder whether PDE inhibitors might represent new therapeutic approaches for preventing and treating MetS.
Keywords	adenosine monophosphate ; blood ; cell proliferation ; cholesterol ; cyclic AMP ; cyclic GMP ; diabetes mellitus ; enzymes ; heart diseases ; hypertension ; inflammation ; metabolic syndrome ; oxidative stress ; risk
Language	English
Dates of publication	2011-12
Size	p. 698-706.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2011.09.012
Database	NAL-Catalogue (AGRICOLA)

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Article: Cyclic nucleotide phosphodiesterase (PDE) superfamily: a new target for the development of specific therapeutic agents.

Lugnier, Claire

Pharmacology & therapeutics

2006 Volume 109, Issue 3, Page(s) 366–398

Abstract: Cyclic nucleotide phosphodiesterases (PDEs), which are ubiquitously distributed in mammalian tissues, play a major role in cell signaling by hydrolyzing cAMP and cGMP. Due to their diversity, which allows specific distribution at cellular and subcellular ...

Abstract	Cyclic nucleotide phosphodiesterases (PDEs), which are ubiquitously distributed in mammalian tissues, play a major role in cell signaling by hydrolyzing cAMP and cGMP. Due to their diversity, which allows specific distribution at cellular and subcellular levels, PDEs can selectively regulate various cellular functions. Their critical role in intracellular signaling has recently designated them as new therapeutic targets for inflammation. The PDE superfamily represents 11 gene families (PDE1 to PDE11). Each family encompasses 1 to 4 distinct genes, to give more than 20 genes in mammals encoding the more than 50 different PDE proteins probably produced in mammalian cells. Although PDE1 to PDE6 were the first well-characterized isoforms because of their predominance in various tissues and cells, their specific contribution to tissue function and their regulation in pathophysiology remain open research fields. This concerns particularly the newly discovered families, PDE7 to PDE11, for which roles are not yet established. In many pathologies, such as inflammation, neurodegeneration, and cancer, alterations in intracellular signaling related to PDE deregulation may explain the difficulties observed in the prevention and treatment of these pathologies. By inhibiting specifically the up-regulated PDE isozyme(s) with newly synthesized potent and isozyme-selective PDE inhibitors, it may be potentially possible to restore normal intracellular signaling selectively, providing therapy with reduced adverse effects.
MeSH term(s)	Animals ; Cardiovascular System/metabolism ; Cell Proliferation ; Cyclic AMP/metabolism ; Cyclic GMP/metabolism ; Endothelial Cells/cytology ; Humans ; Phosphodiesterase Inhibitors/pharmacology ; Phosphoric Diester Hydrolases/metabolism
Chemical Substances	Phosphodiesterase Inhibitors ; Cyclic AMP (E0399OZS9N) ; Phosphoric Diester Hydrolases (EC 3.1.4.-) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2006-03
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.2005.07.003
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