Cardiac Role of Cyclic-GMP Hydrolyzing Phosphodiesterase Type 5: From Experimental Models to Clinical Trials
Abstract Cyclic guanosine monophosphate (cGMP) and its primary signaling kinase, protein kinase G, play an important role in counterbalancing stress remodeling in the heart. Growing evidence supports a positive impact on a variety of cardiac disease conditions from the suppression of cGMP hydrolysis...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kass, David A. [verfasserIn] |
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| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2012 |
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| Schlagwörter: |
Cyclic guanosine monophosphate Cyclic GMP-dependent protein kinase |
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| Übergeordnetes Werk: |
Enthalten in: Current heart failure reports - Philadelphia, Pa. : Current Science, 2004, 9(2012), 3 vom: 15. Juli, Seite 192-199 |
|---|---|
| Übergeordnetes Werk: |
volume:9 ; year:2012 ; number:3 ; day:15 ; month:07 ; pages:192-199 |
| Links: |
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| DOI / URN: |
10.1007/s11897-012-0101-0 |
|---|
| Katalog-ID: |
SPR022921400 |
|---|
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| 520 | |a Abstract Cyclic guanosine monophosphate (cGMP) and its primary signaling kinase, protein kinase G, play an important role in counterbalancing stress remodeling in the heart. Growing evidence supports a positive impact on a variety of cardiac disease conditions from the suppression of cGMP hydrolysis. The latter is regulated by members of the phosphodiesterase (PDE) superfamily, of which cGMP-selective PDE5 has been best studied. Inhibitors such as sildenafil and tadalafil ameliorate cardiac pressure and volume overload, ischemic injury, and cardiotoxicity. Clinical trials have begun exploring their potential to benefit dilated cardiomyopathy and heart failure with a preserved ejection fraction. This review discusses recent developments in the field, highlighting basic science and clinical studies. | ||
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| 650 | 4 | |a Protein kinase G |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Cyclic GMP-dependent protein kinase |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Phosphodiesterase |7 (dpeaa)DE-He213 | |
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| 650 | 4 | |a Hypertrophy |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Ventricular function |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Remodeling |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Fibrosis |7 (dpeaa)DE-He213 | |
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| 912 | |a GBV_ILN_2031 | ||
| 912 | |a GBV_ILN_2034 | ||
| 912 | |a GBV_ILN_2037 | ||
| 912 | |a GBV_ILN_2038 | ||
| 912 | |a GBV_ILN_2039 | ||
| 912 | |a GBV_ILN_2044 | ||
| 912 | |a GBV_ILN_2048 | ||
| 912 | |a GBV_ILN_2049 | ||
| 912 | |a GBV_ILN_2050 | ||
| 912 | |a GBV_ILN_2055 | ||
| 912 | |a GBV_ILN_2057 | ||
| 912 | |a GBV_ILN_2059 | ||
| 912 | |a GBV_ILN_2061 | ||
| 912 | |a GBV_ILN_2064 | ||
| 912 | |a GBV_ILN_2065 | ||
| 912 | |a GBV_ILN_2068 | ||
| 912 | |a GBV_ILN_2070 | ||
| 912 | |a GBV_ILN_2086 | ||
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| 912 | |a GBV_ILN_2122 | ||
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| 912 | |a GBV_ILN_2144 | ||
| 912 | |a GBV_ILN_2147 | ||
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| 912 | |a GBV_ILN_2152 | ||
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| 912 | |a GBV_ILN_2446 | ||
| 912 | |a GBV_ILN_2470 | ||
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| 912 | |a GBV_ILN_2507 | ||
| 912 | |a GBV_ILN_2522 | ||
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| 912 | |a GBV_ILN_4035 | ||
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10.1007/s11897-012-0101-0 doi (DE-627)SPR022921400 (SPR)s11897-012-0101-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Kass, David A. verfasserin aut Cardiac Role of Cyclic-GMP Hydrolyzing Phosphodiesterase Type 5: From Experimental Models to Clinical Trials 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Cyclic guanosine monophosphate (cGMP) and its primary signaling kinase, protein kinase G, play an important role in counterbalancing stress remodeling in the heart. Growing evidence supports a positive impact on a variety of cardiac disease conditions from the suppression of cGMP hydrolysis. The latter is regulated by members of the phosphodiesterase (PDE) superfamily, of which cGMP-selective PDE5 has been best studied. Inhibitors such as sildenafil and tadalafil ameliorate cardiac pressure and volume overload, ischemic injury, and cardiotoxicity. Clinical trials have begun exploring their potential to benefit dilated cardiomyopathy and heart failure with a preserved ejection fraction. This review discusses recent developments in the field, highlighting basic science and clinical studies. Cyclic guanosine monophosphate (dpeaa)DE-He213 Protein kinase G (dpeaa)DE-He213 Cyclic GMP-dependent protein kinase (dpeaa)DE-He213 Phosphodiesterase (dpeaa)DE-He213 PDE5 (dpeaa)DE-He213 PDE2 (dpeaa)DE-He213 PDE1 (dpeaa)DE-He213 Sildenafil (dpeaa)DE-He213 Tadalafil (dpeaa)DE-He213 Heart failure (dpeaa)DE-He213 Hypertrophy (dpeaa)DE-He213 Ventricular function (dpeaa)DE-He213 Remodeling (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Transforming growth factor beta (dpeaa)DE-He213 Cyclic AMP (dpeaa)DE-He213 Signal transduction (dpeaa)DE-He213 RGS2 (dpeaa)DE-He213 TRPC channel (dpeaa)DE-He213 Ischemia (dpeaa)DE-He213 Preconditioning (dpeaa)DE-He213 Mitochondria (dpeaa)DE-He213 Human (dpeaa)DE-He213 Genetic models (dpeaa)DE-He213 Enthalten in Current heart failure reports Philadelphia, Pa. : Current Science, 2004 9(2012), 3 vom: 15. Juli, Seite 192-199 (DE-627)479466890 (DE-600)2177075-X 1546-9549 nnns volume:9 year:2012 number:3 day:15 month:07 pages:192-199 https://dx.doi.org/10.1007/s11897-012-0101-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.85 ASE AR 9 2012 3 15 07 192-199 |
| spelling |
10.1007/s11897-012-0101-0 doi (DE-627)SPR022921400 (SPR)s11897-012-0101-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Kass, David A. verfasserin aut Cardiac Role of Cyclic-GMP Hydrolyzing Phosphodiesterase Type 5: From Experimental Models to Clinical Trials 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Cyclic guanosine monophosphate (cGMP) and its primary signaling kinase, protein kinase G, play an important role in counterbalancing stress remodeling in the heart. Growing evidence supports a positive impact on a variety of cardiac disease conditions from the suppression of cGMP hydrolysis. The latter is regulated by members of the phosphodiesterase (PDE) superfamily, of which cGMP-selective PDE5 has been best studied. Inhibitors such as sildenafil and tadalafil ameliorate cardiac pressure and volume overload, ischemic injury, and cardiotoxicity. Clinical trials have begun exploring their potential to benefit dilated cardiomyopathy and heart failure with a preserved ejection fraction. This review discusses recent developments in the field, highlighting basic science and clinical studies. Cyclic guanosine monophosphate (dpeaa)DE-He213 Protein kinase G (dpeaa)DE-He213 Cyclic GMP-dependent protein kinase (dpeaa)DE-He213 Phosphodiesterase (dpeaa)DE-He213 PDE5 (dpeaa)DE-He213 PDE2 (dpeaa)DE-He213 PDE1 (dpeaa)DE-He213 Sildenafil (dpeaa)DE-He213 Tadalafil (dpeaa)DE-He213 Heart failure (dpeaa)DE-He213 Hypertrophy (dpeaa)DE-He213 Ventricular function (dpeaa)DE-He213 Remodeling (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Transforming growth factor beta (dpeaa)DE-He213 Cyclic AMP (dpeaa)DE-He213 Signal transduction (dpeaa)DE-He213 RGS2 (dpeaa)DE-He213 TRPC channel (dpeaa)DE-He213 Ischemia (dpeaa)DE-He213 Preconditioning (dpeaa)DE-He213 Mitochondria (dpeaa)DE-He213 Human (dpeaa)DE-He213 Genetic models (dpeaa)DE-He213 Enthalten in Current heart failure reports Philadelphia, Pa. : Current Science, 2004 9(2012), 3 vom: 15. Juli, Seite 192-199 (DE-627)479466890 (DE-600)2177075-X 1546-9549 nnns volume:9 year:2012 number:3 day:15 month:07 pages:192-199 https://dx.doi.org/10.1007/s11897-012-0101-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.85 ASE AR 9 2012 3 15 07 192-199 |
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10.1007/s11897-012-0101-0 doi (DE-627)SPR022921400 (SPR)s11897-012-0101-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Kass, David A. verfasserin aut Cardiac Role of Cyclic-GMP Hydrolyzing Phosphodiesterase Type 5: From Experimental Models to Clinical Trials 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Cyclic guanosine monophosphate (cGMP) and its primary signaling kinase, protein kinase G, play an important role in counterbalancing stress remodeling in the heart. Growing evidence supports a positive impact on a variety of cardiac disease conditions from the suppression of cGMP hydrolysis. The latter is regulated by members of the phosphodiesterase (PDE) superfamily, of which cGMP-selective PDE5 has been best studied. Inhibitors such as sildenafil and tadalafil ameliorate cardiac pressure and volume overload, ischemic injury, and cardiotoxicity. Clinical trials have begun exploring their potential to benefit dilated cardiomyopathy and heart failure with a preserved ejection fraction. This review discusses recent developments in the field, highlighting basic science and clinical studies. Cyclic guanosine monophosphate (dpeaa)DE-He213 Protein kinase G (dpeaa)DE-He213 Cyclic GMP-dependent protein kinase (dpeaa)DE-He213 Phosphodiesterase (dpeaa)DE-He213 PDE5 (dpeaa)DE-He213 PDE2 (dpeaa)DE-He213 PDE1 (dpeaa)DE-He213 Sildenafil (dpeaa)DE-He213 Tadalafil (dpeaa)DE-He213 Heart failure (dpeaa)DE-He213 Hypertrophy (dpeaa)DE-He213 Ventricular function (dpeaa)DE-He213 Remodeling (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Transforming growth factor beta (dpeaa)DE-He213 Cyclic AMP (dpeaa)DE-He213 Signal transduction (dpeaa)DE-He213 RGS2 (dpeaa)DE-He213 TRPC channel (dpeaa)DE-He213 Ischemia (dpeaa)DE-He213 Preconditioning (dpeaa)DE-He213 Mitochondria (dpeaa)DE-He213 Human (dpeaa)DE-He213 Genetic models (dpeaa)DE-He213 Enthalten in Current heart failure reports Philadelphia, Pa. : Current Science, 2004 9(2012), 3 vom: 15. Juli, Seite 192-199 (DE-627)479466890 (DE-600)2177075-X 1546-9549 nnns volume:9 year:2012 number:3 day:15 month:07 pages:192-199 https://dx.doi.org/10.1007/s11897-012-0101-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.85 ASE AR 9 2012 3 15 07 192-199 |
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10.1007/s11897-012-0101-0 doi (DE-627)SPR022921400 (SPR)s11897-012-0101-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Kass, David A. verfasserin aut Cardiac Role of Cyclic-GMP Hydrolyzing Phosphodiesterase Type 5: From Experimental Models to Clinical Trials 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Cyclic guanosine monophosphate (cGMP) and its primary signaling kinase, protein kinase G, play an important role in counterbalancing stress remodeling in the heart. Growing evidence supports a positive impact on a variety of cardiac disease conditions from the suppression of cGMP hydrolysis. The latter is regulated by members of the phosphodiesterase (PDE) superfamily, of which cGMP-selective PDE5 has been best studied. Inhibitors such as sildenafil and tadalafil ameliorate cardiac pressure and volume overload, ischemic injury, and cardiotoxicity. Clinical trials have begun exploring their potential to benefit dilated cardiomyopathy and heart failure with a preserved ejection fraction. This review discusses recent developments in the field, highlighting basic science and clinical studies. Cyclic guanosine monophosphate (dpeaa)DE-He213 Protein kinase G (dpeaa)DE-He213 Cyclic GMP-dependent protein kinase (dpeaa)DE-He213 Phosphodiesterase (dpeaa)DE-He213 PDE5 (dpeaa)DE-He213 PDE2 (dpeaa)DE-He213 PDE1 (dpeaa)DE-He213 Sildenafil (dpeaa)DE-He213 Tadalafil (dpeaa)DE-He213 Heart failure (dpeaa)DE-He213 Hypertrophy (dpeaa)DE-He213 Ventricular function (dpeaa)DE-He213 Remodeling (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Transforming growth factor beta (dpeaa)DE-He213 Cyclic AMP (dpeaa)DE-He213 Signal transduction (dpeaa)DE-He213 RGS2 (dpeaa)DE-He213 TRPC channel (dpeaa)DE-He213 Ischemia (dpeaa)DE-He213 Preconditioning (dpeaa)DE-He213 Mitochondria (dpeaa)DE-He213 Human (dpeaa)DE-He213 Genetic models (dpeaa)DE-He213 Enthalten in Current heart failure reports Philadelphia, Pa. : Current Science, 2004 9(2012), 3 vom: 15. Juli, Seite 192-199 (DE-627)479466890 (DE-600)2177075-X 1546-9549 nnns volume:9 year:2012 number:3 day:15 month:07 pages:192-199 https://dx.doi.org/10.1007/s11897-012-0101-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.85 ASE AR 9 2012 3 15 07 192-199 |
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10.1007/s11897-012-0101-0 doi (DE-627)SPR022921400 (SPR)s11897-012-0101-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Kass, David A. verfasserin aut Cardiac Role of Cyclic-GMP Hydrolyzing Phosphodiesterase Type 5: From Experimental Models to Clinical Trials 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Cyclic guanosine monophosphate (cGMP) and its primary signaling kinase, protein kinase G, play an important role in counterbalancing stress remodeling in the heart. Growing evidence supports a positive impact on a variety of cardiac disease conditions from the suppression of cGMP hydrolysis. The latter is regulated by members of the phosphodiesterase (PDE) superfamily, of which cGMP-selective PDE5 has been best studied. Inhibitors such as sildenafil and tadalafil ameliorate cardiac pressure and volume overload, ischemic injury, and cardiotoxicity. Clinical trials have begun exploring their potential to benefit dilated cardiomyopathy and heart failure with a preserved ejection fraction. This review discusses recent developments in the field, highlighting basic science and clinical studies. Cyclic guanosine monophosphate (dpeaa)DE-He213 Protein kinase G (dpeaa)DE-He213 Cyclic GMP-dependent protein kinase (dpeaa)DE-He213 Phosphodiesterase (dpeaa)DE-He213 PDE5 (dpeaa)DE-He213 PDE2 (dpeaa)DE-He213 PDE1 (dpeaa)DE-He213 Sildenafil (dpeaa)DE-He213 Tadalafil (dpeaa)DE-He213 Heart failure (dpeaa)DE-He213 Hypertrophy (dpeaa)DE-He213 Ventricular function (dpeaa)DE-He213 Remodeling (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Transforming growth factor beta (dpeaa)DE-He213 Cyclic AMP (dpeaa)DE-He213 Signal transduction (dpeaa)DE-He213 RGS2 (dpeaa)DE-He213 TRPC channel (dpeaa)DE-He213 Ischemia (dpeaa)DE-He213 Preconditioning (dpeaa)DE-He213 Mitochondria (dpeaa)DE-He213 Human (dpeaa)DE-He213 Genetic models (dpeaa)DE-He213 Enthalten in Current heart failure reports Philadelphia, Pa. : Current Science, 2004 9(2012), 3 vom: 15. Juli, Seite 192-199 (DE-627)479466890 (DE-600)2177075-X 1546-9549 nnns volume:9 year:2012 number:3 day:15 month:07 pages:192-199 https://dx.doi.org/10.1007/s11897-012-0101-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.85 ASE AR 9 2012 3 15 07 192-199 |
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Enthalten in Current heart failure reports 9(2012), 3 vom: 15. Juli, Seite 192-199 volume:9 year:2012 number:3 day:15 month:07 pages:192-199 |
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Cyclic guanosine monophosphate Protein kinase G Cyclic GMP-dependent protein kinase Phosphodiesterase PDE5 PDE2 PDE1 Sildenafil Tadalafil Heart failure Hypertrophy Ventricular function Remodeling Fibrosis Transforming growth factor beta Cyclic AMP Signal transduction RGS2 TRPC channel Ischemia Preconditioning Mitochondria Human Genetic models |
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Kass, David A. @@aut@@ |
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|
| author |
Kass, David A. |
| spellingShingle |
Kass, David A. ddc 610 bkl 44.85 misc Cyclic guanosine monophosphate misc Protein kinase G misc Cyclic GMP-dependent protein kinase misc Phosphodiesterase misc PDE5 misc PDE2 misc PDE1 misc Sildenafil misc Tadalafil misc Heart failure misc Hypertrophy misc Ventricular function misc Remodeling misc Fibrosis misc Transforming growth factor beta misc Cyclic AMP misc Signal transduction misc RGS2 misc TRPC channel misc Ischemia misc Preconditioning misc Mitochondria misc Human misc Genetic models Cardiac Role of Cyclic-GMP Hydrolyzing Phosphodiesterase Type 5: From Experimental Models to Clinical Trials |
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Kass, David A. |
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@@773@@(DE-627)479466890 |
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electronic Article |
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610 - Medicine & health |
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keep |
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springer |
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true |
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Not Illustrated |
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1546-9549 |
| topic_title |
610 ASE 44.85 bkl Cardiac Role of Cyclic-GMP Hydrolyzing Phosphodiesterase Type 5: From Experimental Models to Clinical Trials Cyclic guanosine monophosphate (dpeaa)DE-He213 Protein kinase G (dpeaa)DE-He213 Cyclic GMP-dependent protein kinase (dpeaa)DE-He213 Phosphodiesterase (dpeaa)DE-He213 PDE5 (dpeaa)DE-He213 PDE2 (dpeaa)DE-He213 PDE1 (dpeaa)DE-He213 Sildenafil (dpeaa)DE-He213 Tadalafil (dpeaa)DE-He213 Heart failure (dpeaa)DE-He213 Hypertrophy (dpeaa)DE-He213 Ventricular function (dpeaa)DE-He213 Remodeling (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Transforming growth factor beta (dpeaa)DE-He213 Cyclic AMP (dpeaa)DE-He213 Signal transduction (dpeaa)DE-He213 RGS2 (dpeaa)DE-He213 TRPC channel (dpeaa)DE-He213 Ischemia (dpeaa)DE-He213 Preconditioning (dpeaa)DE-He213 Mitochondria (dpeaa)DE-He213 Human (dpeaa)DE-He213 Genetic models (dpeaa)DE-He213 |
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ddc 610 bkl 44.85 misc Cyclic guanosine monophosphate misc Protein kinase G misc Cyclic GMP-dependent protein kinase misc Phosphodiesterase misc PDE5 misc PDE2 misc PDE1 misc Sildenafil misc Tadalafil misc Heart failure misc Hypertrophy misc Ventricular function misc Remodeling misc Fibrosis misc Transforming growth factor beta misc Cyclic AMP misc Signal transduction misc RGS2 misc TRPC channel misc Ischemia misc Preconditioning misc Mitochondria misc Human misc Genetic models |
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ddc 610 bkl 44.85 misc Cyclic guanosine monophosphate misc Protein kinase G misc Cyclic GMP-dependent protein kinase misc Phosphodiesterase misc PDE5 misc PDE2 misc PDE1 misc Sildenafil misc Tadalafil misc Heart failure misc Hypertrophy misc Ventricular function misc Remodeling misc Fibrosis misc Transforming growth factor beta misc Cyclic AMP misc Signal transduction misc RGS2 misc TRPC channel misc Ischemia misc Preconditioning misc Mitochondria misc Human misc Genetic models |
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ddc 610 bkl 44.85 misc Cyclic guanosine monophosphate misc Protein kinase G misc Cyclic GMP-dependent protein kinase misc Phosphodiesterase misc PDE5 misc PDE2 misc PDE1 misc Sildenafil misc Tadalafil misc Heart failure misc Hypertrophy misc Ventricular function misc Remodeling misc Fibrosis misc Transforming growth factor beta misc Cyclic AMP misc Signal transduction misc RGS2 misc TRPC channel misc Ischemia misc Preconditioning misc Mitochondria misc Human misc Genetic models |
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cardiac role of cyclic-gmp hydrolyzing phosphodiesterase type 5: from experimental models to clinical trials |
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Cardiac Role of Cyclic-GMP Hydrolyzing Phosphodiesterase Type 5: From Experimental Models to Clinical Trials |
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Abstract Cyclic guanosine monophosphate (cGMP) and its primary signaling kinase, protein kinase G, play an important role in counterbalancing stress remodeling in the heart. Growing evidence supports a positive impact on a variety of cardiac disease conditions from the suppression of cGMP hydrolysis. The latter is regulated by members of the phosphodiesterase (PDE) superfamily, of which cGMP-selective PDE5 has been best studied. Inhibitors such as sildenafil and tadalafil ameliorate cardiac pressure and volume overload, ischemic injury, and cardiotoxicity. Clinical trials have begun exploring their potential to benefit dilated cardiomyopathy and heart failure with a preserved ejection fraction. This review discusses recent developments in the field, highlighting basic science and clinical studies. |
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Abstract Cyclic guanosine monophosphate (cGMP) and its primary signaling kinase, protein kinase G, play an important role in counterbalancing stress remodeling in the heart. Growing evidence supports a positive impact on a variety of cardiac disease conditions from the suppression of cGMP hydrolysis. The latter is regulated by members of the phosphodiesterase (PDE) superfamily, of which cGMP-selective PDE5 has been best studied. Inhibitors such as sildenafil and tadalafil ameliorate cardiac pressure and volume overload, ischemic injury, and cardiotoxicity. Clinical trials have begun exploring their potential to benefit dilated cardiomyopathy and heart failure with a preserved ejection fraction. This review discusses recent developments in the field, highlighting basic science and clinical studies. |
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Abstract Cyclic guanosine monophosphate (cGMP) and its primary signaling kinase, protein kinase G, play an important role in counterbalancing stress remodeling in the heart. Growing evidence supports a positive impact on a variety of cardiac disease conditions from the suppression of cGMP hydrolysis. The latter is regulated by members of the phosphodiesterase (PDE) superfamily, of which cGMP-selective PDE5 has been best studied. Inhibitors such as sildenafil and tadalafil ameliorate cardiac pressure and volume overload, ischemic injury, and cardiotoxicity. Clinical trials have begun exploring their potential to benefit dilated cardiomyopathy and heart failure with a preserved ejection fraction. This review discusses recent developments in the field, highlighting basic science and clinical studies. |
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| score |
7.4027348 |