An Emerging Role of Degrading Proteinases in Hypertension and the Metabolic Syndrome: Autodigestion and Receptor Cleavage
Abstract One of the major challenges for hypertension research is to identify the mechanisms that cause the comorbidities encountered in many hypertensive patients, as seen in the metabolic syndrome. An emerging body of evidence suggests that human and experimental hypertensives may exhibit uncontro...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Schmid-Schönbein, Geert W. [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2011 |
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| Schlagwörter: |
Vascular endothelial growth factor receptor |
|---|
| Übergeordnetes Werk: |
Enthalten in: Current hypertension reports - Philadelphia, Pa. : Current Science Inc., 1999, 14(2011), 1 vom: 12. Nov., Seite 88-96 |
|---|---|
| Übergeordnetes Werk: |
volume:14 ; year:2011 ; number:1 ; day:12 ; month:11 ; pages:88-96 |
| Links: |
|---|
| DOI / URN: |
10.1007/s11906-011-0240-9 |
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SPR02294978X |
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| 520 | |a Abstract One of the major challenges for hypertension research is to identify the mechanisms that cause the comorbidities encountered in many hypertensive patients, as seen in the metabolic syndrome. An emerging body of evidence suggests that human and experimental hypertensives may exhibit uncontrolled activity of proteinases, including the family of matrix metalloproteinases, recognized for their ability to restructure the extracellular matrix proteins and to play a role in hypertrophy. We propose a new hypothesis that provides a molecular framework for the comorbidities of hypertension, diabetes, capillary rarefaction, immune suppression, and other cell and organ dysfunctions due to early and uncontrolled extracellular receptor cleavage by active proteinases. The proteinase and signaling activity in hypertensives requires further detailed analysis of the proteinase expression, the mechanisms causing proenzyme activation, and identification of the proteinase substrate. This work may open the opportunity for reassessment of old interventions and development of new interventions to manage hypertension and its comorbidities. | ||
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| 650 | 4 | |a Metabolic syndrome |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Hypertrophy |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Insulin resistance |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Capillary rarefaction |7 (dpeaa)DE-He213 | |
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| 650 | 4 | |a Vascular endothelial growth factor receptor |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a NF-kappaB |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Spontaneously hypertensive rat |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Essential hypertension |7 (dpeaa)DE-He213 | |
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10.1007/s11906-011-0240-9 doi (DE-627)SPR02294978X (SPR)s11906-011-0240-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Schmid-Schönbein, Geert W. verfasserin aut An Emerging Role of Degrading Proteinases in Hypertension and the Metabolic Syndrome: Autodigestion and Receptor Cleavage 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract One of the major challenges for hypertension research is to identify the mechanisms that cause the comorbidities encountered in many hypertensive patients, as seen in the metabolic syndrome. An emerging body of evidence suggests that human and experimental hypertensives may exhibit uncontrolled activity of proteinases, including the family of matrix metalloproteinases, recognized for their ability to restructure the extracellular matrix proteins and to play a role in hypertrophy. We propose a new hypothesis that provides a molecular framework for the comorbidities of hypertension, diabetes, capillary rarefaction, immune suppression, and other cell and organ dysfunctions due to early and uncontrolled extracellular receptor cleavage by active proteinases. The proteinase and signaling activity in hypertensives requires further detailed analysis of the proteinase expression, the mechanisms causing proenzyme activation, and identification of the proteinase substrate. This work may open the opportunity for reassessment of old interventions and development of new interventions to manage hypertension and its comorbidities. Matrix metalloproteinase (dpeaa)DE-He213 MMP (dpeaa)DE-He213 ADAM (dpeaa)DE-He213 Metabolic syndrome (dpeaa)DE-He213 Hypertrophy (dpeaa)DE-He213 Insulin resistance (dpeaa)DE-He213 Capillary rarefaction (dpeaa)DE-He213 Immune suppression (dpeaa)DE-He213 Insulin receptor (dpeaa)DE-He213 Beta-adrenergic receptor (dpeaa)DE-He213 Vascular endothelial growth factor receptor (dpeaa)DE-He213 NF-kappaB (dpeaa)DE-He213 Spontaneously hypertensive rat (dpeaa)DE-He213 Essential hypertension (dpeaa)DE-He213 Microcirculation (dpeaa)DE-He213 Artery (dpeaa)DE-He213 Arteriole (dpeaa)DE-He213 Extracellular matrix protein (dpeaa)DE-He213 Proteinase inhibitor (dpeaa)DE-He213 Angiotensin-converting enzyme (dpeaa)DE-He213 Angiotensin (dpeaa)DE-He213 Hypertension (dpeaa)DE-He213 Metabolic syndrome (dpeaa)DE-He213 Pathogenesis (dpeaa)DE-He213 Enthalten in Current hypertension reports Philadelphia, Pa. : Current Science Inc., 1999 14(2011), 1 vom: 12. Nov., Seite 88-96 (DE-627)357168283 (DE-600)2094165-1 1534-3111 nnns volume:14 year:2011 number:1 day:12 month:11 pages:88-96 https://dx.doi.org/10.1007/s11906-011-0240-9 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 14 2011 1 12 11 88-96 |
| spelling |
10.1007/s11906-011-0240-9 doi (DE-627)SPR02294978X (SPR)s11906-011-0240-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Schmid-Schönbein, Geert W. verfasserin aut An Emerging Role of Degrading Proteinases in Hypertension and the Metabolic Syndrome: Autodigestion and Receptor Cleavage 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract One of the major challenges for hypertension research is to identify the mechanisms that cause the comorbidities encountered in many hypertensive patients, as seen in the metabolic syndrome. An emerging body of evidence suggests that human and experimental hypertensives may exhibit uncontrolled activity of proteinases, including the family of matrix metalloproteinases, recognized for their ability to restructure the extracellular matrix proteins and to play a role in hypertrophy. We propose a new hypothesis that provides a molecular framework for the comorbidities of hypertension, diabetes, capillary rarefaction, immune suppression, and other cell and organ dysfunctions due to early and uncontrolled extracellular receptor cleavage by active proteinases. The proteinase and signaling activity in hypertensives requires further detailed analysis of the proteinase expression, the mechanisms causing proenzyme activation, and identification of the proteinase substrate. This work may open the opportunity for reassessment of old interventions and development of new interventions to manage hypertension and its comorbidities. Matrix metalloproteinase (dpeaa)DE-He213 MMP (dpeaa)DE-He213 ADAM (dpeaa)DE-He213 Metabolic syndrome (dpeaa)DE-He213 Hypertrophy (dpeaa)DE-He213 Insulin resistance (dpeaa)DE-He213 Capillary rarefaction (dpeaa)DE-He213 Immune suppression (dpeaa)DE-He213 Insulin receptor (dpeaa)DE-He213 Beta-adrenergic receptor (dpeaa)DE-He213 Vascular endothelial growth factor receptor (dpeaa)DE-He213 NF-kappaB (dpeaa)DE-He213 Spontaneously hypertensive rat (dpeaa)DE-He213 Essential hypertension (dpeaa)DE-He213 Microcirculation (dpeaa)DE-He213 Artery (dpeaa)DE-He213 Arteriole (dpeaa)DE-He213 Extracellular matrix protein (dpeaa)DE-He213 Proteinase inhibitor (dpeaa)DE-He213 Angiotensin-converting enzyme (dpeaa)DE-He213 Angiotensin (dpeaa)DE-He213 Hypertension (dpeaa)DE-He213 Metabolic syndrome (dpeaa)DE-He213 Pathogenesis (dpeaa)DE-He213 Enthalten in Current hypertension reports Philadelphia, Pa. : Current Science Inc., 1999 14(2011), 1 vom: 12. Nov., Seite 88-96 (DE-627)357168283 (DE-600)2094165-1 1534-3111 nnns volume:14 year:2011 number:1 day:12 month:11 pages:88-96 https://dx.doi.org/10.1007/s11906-011-0240-9 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 14 2011 1 12 11 88-96 |
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10.1007/s11906-011-0240-9 doi (DE-627)SPR02294978X (SPR)s11906-011-0240-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Schmid-Schönbein, Geert W. verfasserin aut An Emerging Role of Degrading Proteinases in Hypertension and the Metabolic Syndrome: Autodigestion and Receptor Cleavage 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract One of the major challenges for hypertension research is to identify the mechanisms that cause the comorbidities encountered in many hypertensive patients, as seen in the metabolic syndrome. An emerging body of evidence suggests that human and experimental hypertensives may exhibit uncontrolled activity of proteinases, including the family of matrix metalloproteinases, recognized for their ability to restructure the extracellular matrix proteins and to play a role in hypertrophy. We propose a new hypothesis that provides a molecular framework for the comorbidities of hypertension, diabetes, capillary rarefaction, immune suppression, and other cell and organ dysfunctions due to early and uncontrolled extracellular receptor cleavage by active proteinases. The proteinase and signaling activity in hypertensives requires further detailed analysis of the proteinase expression, the mechanisms causing proenzyme activation, and identification of the proteinase substrate. This work may open the opportunity for reassessment of old interventions and development of new interventions to manage hypertension and its comorbidities. Matrix metalloproteinase (dpeaa)DE-He213 MMP (dpeaa)DE-He213 ADAM (dpeaa)DE-He213 Metabolic syndrome (dpeaa)DE-He213 Hypertrophy (dpeaa)DE-He213 Insulin resistance (dpeaa)DE-He213 Capillary rarefaction (dpeaa)DE-He213 Immune suppression (dpeaa)DE-He213 Insulin receptor (dpeaa)DE-He213 Beta-adrenergic receptor (dpeaa)DE-He213 Vascular endothelial growth factor receptor (dpeaa)DE-He213 NF-kappaB (dpeaa)DE-He213 Spontaneously hypertensive rat (dpeaa)DE-He213 Essential hypertension (dpeaa)DE-He213 Microcirculation (dpeaa)DE-He213 Artery (dpeaa)DE-He213 Arteriole (dpeaa)DE-He213 Extracellular matrix protein (dpeaa)DE-He213 Proteinase inhibitor (dpeaa)DE-He213 Angiotensin-converting enzyme (dpeaa)DE-He213 Angiotensin (dpeaa)DE-He213 Hypertension (dpeaa)DE-He213 Metabolic syndrome (dpeaa)DE-He213 Pathogenesis (dpeaa)DE-He213 Enthalten in Current hypertension reports Philadelphia, Pa. : Current Science Inc., 1999 14(2011), 1 vom: 12. Nov., Seite 88-96 (DE-627)357168283 (DE-600)2094165-1 1534-3111 nnns volume:14 year:2011 number:1 day:12 month:11 pages:88-96 https://dx.doi.org/10.1007/s11906-011-0240-9 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 14 2011 1 12 11 88-96 |
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10.1007/s11906-011-0240-9 doi (DE-627)SPR02294978X (SPR)s11906-011-0240-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Schmid-Schönbein, Geert W. verfasserin aut An Emerging Role of Degrading Proteinases in Hypertension and the Metabolic Syndrome: Autodigestion and Receptor Cleavage 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract One of the major challenges for hypertension research is to identify the mechanisms that cause the comorbidities encountered in many hypertensive patients, as seen in the metabolic syndrome. An emerging body of evidence suggests that human and experimental hypertensives may exhibit uncontrolled activity of proteinases, including the family of matrix metalloproteinases, recognized for their ability to restructure the extracellular matrix proteins and to play a role in hypertrophy. We propose a new hypothesis that provides a molecular framework for the comorbidities of hypertension, diabetes, capillary rarefaction, immune suppression, and other cell and organ dysfunctions due to early and uncontrolled extracellular receptor cleavage by active proteinases. The proteinase and signaling activity in hypertensives requires further detailed analysis of the proteinase expression, the mechanisms causing proenzyme activation, and identification of the proteinase substrate. This work may open the opportunity for reassessment of old interventions and development of new interventions to manage hypertension and its comorbidities. Matrix metalloproteinase (dpeaa)DE-He213 MMP (dpeaa)DE-He213 ADAM (dpeaa)DE-He213 Metabolic syndrome (dpeaa)DE-He213 Hypertrophy (dpeaa)DE-He213 Insulin resistance (dpeaa)DE-He213 Capillary rarefaction (dpeaa)DE-He213 Immune suppression (dpeaa)DE-He213 Insulin receptor (dpeaa)DE-He213 Beta-adrenergic receptor (dpeaa)DE-He213 Vascular endothelial growth factor receptor (dpeaa)DE-He213 NF-kappaB (dpeaa)DE-He213 Spontaneously hypertensive rat (dpeaa)DE-He213 Essential hypertension (dpeaa)DE-He213 Microcirculation (dpeaa)DE-He213 Artery (dpeaa)DE-He213 Arteriole (dpeaa)DE-He213 Extracellular matrix protein (dpeaa)DE-He213 Proteinase inhibitor (dpeaa)DE-He213 Angiotensin-converting enzyme (dpeaa)DE-He213 Angiotensin (dpeaa)DE-He213 Hypertension (dpeaa)DE-He213 Metabolic syndrome (dpeaa)DE-He213 Pathogenesis (dpeaa)DE-He213 Enthalten in Current hypertension reports Philadelphia, Pa. : Current Science Inc., 1999 14(2011), 1 vom: 12. Nov., Seite 88-96 (DE-627)357168283 (DE-600)2094165-1 1534-3111 nnns volume:14 year:2011 number:1 day:12 month:11 pages:88-96 https://dx.doi.org/10.1007/s11906-011-0240-9 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 14 2011 1 12 11 88-96 |
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10.1007/s11906-011-0240-9 doi (DE-627)SPR02294978X (SPR)s11906-011-0240-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Schmid-Schönbein, Geert W. verfasserin aut An Emerging Role of Degrading Proteinases in Hypertension and the Metabolic Syndrome: Autodigestion and Receptor Cleavage 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract One of the major challenges for hypertension research is to identify the mechanisms that cause the comorbidities encountered in many hypertensive patients, as seen in the metabolic syndrome. An emerging body of evidence suggests that human and experimental hypertensives may exhibit uncontrolled activity of proteinases, including the family of matrix metalloproteinases, recognized for their ability to restructure the extracellular matrix proteins and to play a role in hypertrophy. We propose a new hypothesis that provides a molecular framework for the comorbidities of hypertension, diabetes, capillary rarefaction, immune suppression, and other cell and organ dysfunctions due to early and uncontrolled extracellular receptor cleavage by active proteinases. The proteinase and signaling activity in hypertensives requires further detailed analysis of the proteinase expression, the mechanisms causing proenzyme activation, and identification of the proteinase substrate. This work may open the opportunity for reassessment of old interventions and development of new interventions to manage hypertension and its comorbidities. Matrix metalloproteinase (dpeaa)DE-He213 MMP (dpeaa)DE-He213 ADAM (dpeaa)DE-He213 Metabolic syndrome (dpeaa)DE-He213 Hypertrophy (dpeaa)DE-He213 Insulin resistance (dpeaa)DE-He213 Capillary rarefaction (dpeaa)DE-He213 Immune suppression (dpeaa)DE-He213 Insulin receptor (dpeaa)DE-He213 Beta-adrenergic receptor (dpeaa)DE-He213 Vascular endothelial growth factor receptor (dpeaa)DE-He213 NF-kappaB (dpeaa)DE-He213 Spontaneously hypertensive rat (dpeaa)DE-He213 Essential hypertension (dpeaa)DE-He213 Microcirculation (dpeaa)DE-He213 Artery (dpeaa)DE-He213 Arteriole (dpeaa)DE-He213 Extracellular matrix protein (dpeaa)DE-He213 Proteinase inhibitor (dpeaa)DE-He213 Angiotensin-converting enzyme (dpeaa)DE-He213 Angiotensin (dpeaa)DE-He213 Hypertension (dpeaa)DE-He213 Metabolic syndrome (dpeaa)DE-He213 Pathogenesis (dpeaa)DE-He213 Enthalten in Current hypertension reports Philadelphia, Pa. : Current Science Inc., 1999 14(2011), 1 vom: 12. Nov., Seite 88-96 (DE-627)357168283 (DE-600)2094165-1 1534-3111 nnns volume:14 year:2011 number:1 day:12 month:11 pages:88-96 https://dx.doi.org/10.1007/s11906-011-0240-9 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 14 2011 1 12 11 88-96 |
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Matrix metalloproteinase MMP ADAM Metabolic syndrome Hypertrophy Insulin resistance Capillary rarefaction Immune suppression Insulin receptor Beta-adrenergic receptor Vascular endothelial growth factor receptor NF-kappaB Spontaneously hypertensive rat Essential hypertension Microcirculation Artery Arteriole Extracellular matrix protein Proteinase inhibitor Angiotensin-converting enzyme Angiotensin Hypertension Pathogenesis |
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An emerging body of evidence suggests that human and experimental hypertensives may exhibit uncontrolled activity of proteinases, including the family of matrix metalloproteinases, recognized for their ability to restructure the extracellular matrix proteins and to play a role in hypertrophy. We propose a new hypothesis that provides a molecular framework for the comorbidities of hypertension, diabetes, capillary rarefaction, immune suppression, and other cell and organ dysfunctions due to early and uncontrolled extracellular receptor cleavage by active proteinases. The proteinase and signaling activity in hypertensives requires further detailed analysis of the proteinase expression, the mechanisms causing proenzyme activation, and identification of the proteinase substrate. 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|
| author |
Schmid-Schönbein, Geert W. |
| spellingShingle |
Schmid-Schönbein, Geert W. ddc 610 bkl 44.85 misc Matrix metalloproteinase misc MMP misc ADAM misc Metabolic syndrome misc Hypertrophy misc Insulin resistance misc Capillary rarefaction misc Immune suppression misc Insulin receptor misc Beta-adrenergic receptor misc Vascular endothelial growth factor receptor misc NF-kappaB misc Spontaneously hypertensive rat misc Essential hypertension misc Microcirculation misc Artery misc Arteriole misc Extracellular matrix protein misc Proteinase inhibitor misc Angiotensin-converting enzyme misc Angiotensin misc Hypertension misc Pathogenesis An Emerging Role of Degrading Proteinases in Hypertension and the Metabolic Syndrome: Autodigestion and Receptor Cleavage |
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Schmid-Schönbein, Geert W. |
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@@773@@(DE-627)357168283 |
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electronic Article |
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610 - Medicine & health |
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keep |
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aut |
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springer |
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true |
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Not Illustrated |
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610 ASE 44.85 bkl An Emerging Role of Degrading Proteinases in Hypertension and the Metabolic Syndrome: Autodigestion and Receptor Cleavage Matrix metalloproteinase (dpeaa)DE-He213 MMP (dpeaa)DE-He213 ADAM (dpeaa)DE-He213 Metabolic syndrome (dpeaa)DE-He213 Hypertrophy (dpeaa)DE-He213 Insulin resistance (dpeaa)DE-He213 Capillary rarefaction (dpeaa)DE-He213 Immune suppression (dpeaa)DE-He213 Insulin receptor (dpeaa)DE-He213 Beta-adrenergic receptor (dpeaa)DE-He213 Vascular endothelial growth factor receptor (dpeaa)DE-He213 NF-kappaB (dpeaa)DE-He213 Spontaneously hypertensive rat (dpeaa)DE-He213 Essential hypertension (dpeaa)DE-He213 Microcirculation (dpeaa)DE-He213 Artery (dpeaa)DE-He213 Arteriole (dpeaa)DE-He213 Extracellular matrix protein (dpeaa)DE-He213 Proteinase inhibitor (dpeaa)DE-He213 Angiotensin-converting enzyme (dpeaa)DE-He213 Angiotensin (dpeaa)DE-He213 Hypertension (dpeaa)DE-He213 Pathogenesis (dpeaa)DE-He213 |
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ddc 610 bkl 44.85 misc Matrix metalloproteinase misc MMP misc ADAM misc Metabolic syndrome misc Hypertrophy misc Insulin resistance misc Capillary rarefaction misc Immune suppression misc Insulin receptor misc Beta-adrenergic receptor misc Vascular endothelial growth factor receptor misc NF-kappaB misc Spontaneously hypertensive rat misc Essential hypertension misc Microcirculation misc Artery misc Arteriole misc Extracellular matrix protein misc Proteinase inhibitor misc Angiotensin-converting enzyme misc Angiotensin misc Hypertension misc Pathogenesis |
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ddc 610 bkl 44.85 misc Matrix metalloproteinase misc MMP misc ADAM misc Metabolic syndrome misc Hypertrophy misc Insulin resistance misc Capillary rarefaction misc Immune suppression misc Insulin receptor misc Beta-adrenergic receptor misc Vascular endothelial growth factor receptor misc NF-kappaB misc Spontaneously hypertensive rat misc Essential hypertension misc Microcirculation misc Artery misc Arteriole misc Extracellular matrix protein misc Proteinase inhibitor misc Angiotensin-converting enzyme misc Angiotensin misc Hypertension misc Pathogenesis |
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An Emerging Role of Degrading Proteinases in Hypertension and the Metabolic Syndrome: Autodigestion and Receptor Cleavage |
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emerging role of degrading proteinases in hypertension and the metabolic syndrome: autodigestion and receptor cleavage |
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An Emerging Role of Degrading Proteinases in Hypertension and the Metabolic Syndrome: Autodigestion and Receptor Cleavage |
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Abstract One of the major challenges for hypertension research is to identify the mechanisms that cause the comorbidities encountered in many hypertensive patients, as seen in the metabolic syndrome. An emerging body of evidence suggests that human and experimental hypertensives may exhibit uncontrolled activity of proteinases, including the family of matrix metalloproteinases, recognized for their ability to restructure the extracellular matrix proteins and to play a role in hypertrophy. We propose a new hypothesis that provides a molecular framework for the comorbidities of hypertension, diabetes, capillary rarefaction, immune suppression, and other cell and organ dysfunctions due to early and uncontrolled extracellular receptor cleavage by active proteinases. The proteinase and signaling activity in hypertensives requires further detailed analysis of the proteinase expression, the mechanisms causing proenzyme activation, and identification of the proteinase substrate. This work may open the opportunity for reassessment of old interventions and development of new interventions to manage hypertension and its comorbidities. |
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Abstract One of the major challenges for hypertension research is to identify the mechanisms that cause the comorbidities encountered in many hypertensive patients, as seen in the metabolic syndrome. An emerging body of evidence suggests that human and experimental hypertensives may exhibit uncontrolled activity of proteinases, including the family of matrix metalloproteinases, recognized for their ability to restructure the extracellular matrix proteins and to play a role in hypertrophy. We propose a new hypothesis that provides a molecular framework for the comorbidities of hypertension, diabetes, capillary rarefaction, immune suppression, and other cell and organ dysfunctions due to early and uncontrolled extracellular receptor cleavage by active proteinases. The proteinase and signaling activity in hypertensives requires further detailed analysis of the proteinase expression, the mechanisms causing proenzyme activation, and identification of the proteinase substrate. This work may open the opportunity for reassessment of old interventions and development of new interventions to manage hypertension and its comorbidities. |
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Abstract One of the major challenges for hypertension research is to identify the mechanisms that cause the comorbidities encountered in many hypertensive patients, as seen in the metabolic syndrome. An emerging body of evidence suggests that human and experimental hypertensives may exhibit uncontrolled activity of proteinases, including the family of matrix metalloproteinases, recognized for their ability to restructure the extracellular matrix proteins and to play a role in hypertrophy. We propose a new hypothesis that provides a molecular framework for the comorbidities of hypertension, diabetes, capillary rarefaction, immune suppression, and other cell and organ dysfunctions due to early and uncontrolled extracellular receptor cleavage by active proteinases. The proteinase and signaling activity in hypertensives requires further detailed analysis of the proteinase expression, the mechanisms causing proenzyme activation, and identification of the proteinase substrate. This work may open the opportunity for reassessment of old interventions and development of new interventions to manage hypertension and its comorbidities. |
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| score |
7.4003353 |