Role of Melanocortin Receptors in the Regulation of Gouty Inflammation
Abstract Gouty arthritis is a form of acute joint inflammation provoked by joint deposition of urate crystals. Although this acute pathology resolves after a few days, the marked degree of inflammation in the joint and—possibly more important to the patient—the excruciating pain it causes require pr...
Ausführliche Beschreibung
Autor*in: |
Montero-Melendez, Trinidad [verfasserIn] Patel, Hetal B. [verfasserIn] Perretti, Mauro [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2011 |
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Schlagwörter: |
Anti-inflammatory therapeutics |
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Übergeordnetes Werk: |
Enthalten in: Current rheumatology reports - Philadelphia, Pa. : Current Science Inc., 1999, 13(2011), 2 vom: 18. Jan., Seite 138-145 |
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Übergeordnetes Werk: |
volume:13 ; year:2011 ; number:2 ; day:18 ; month:01 ; pages:138-145 |
Links: |
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DOI / URN: |
10.1007/s11926-011-0163-0 |
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Katalog-ID: |
SPR023032227 |
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520 | |a Abstract Gouty arthritis is a form of acute joint inflammation provoked by joint deposition of urate crystals. Although this acute pathology resolves after a few days, the marked degree of inflammation in the joint and—possibly more important to the patient—the excruciating pain it causes require proper therapeutic management. Often deemed a “poor sibling” of chronic joint pathologies such as rheumatoid arthritis and psoriatic arthritis, the increasing incidence of gout makes it a more palatable disease for novel drug discovery programs. This fact, associated with novel insights into the molecular mechanisms activated by the urate crystal deposition, is at the basis of new therapeutics under clinical development for gout, a valid example being the effective targeting of the proinflammatory cytokine interleukin-1. Here we briefly review the current status of antigout drug development and propose another target; our focus is on melanocortin receptor agonists as novel therapeutics for gout and inflammatory arthritides, a prototype of which, the adrenocorticotropic hormone, is already used in clinical settings. | ||
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650 | 4 | |a G-protein–coupled receptor |7 (dpeaa)DE-He213 | |
650 | 4 | |a Drug discovery |7 (dpeaa)DE-He213 | |
650 | 4 | |a Gout |7 (dpeaa)DE-He213 | |
650 | 4 | |a Inflammatory arthritis |7 (dpeaa)DE-He213 | |
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650 | 4 | |a Receptor agonists |7 (dpeaa)DE-He213 | |
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10.1007/s11926-011-0163-0 doi (DE-627)SPR023032227 (SPR)s11926-011-0163-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.83 bkl Montero-Melendez, Trinidad verfasserin aut Role of Melanocortin Receptors in the Regulation of Gouty Inflammation 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Gouty arthritis is a form of acute joint inflammation provoked by joint deposition of urate crystals. Although this acute pathology resolves after a few days, the marked degree of inflammation in the joint and—possibly more important to the patient—the excruciating pain it causes require proper therapeutic management. Often deemed a “poor sibling” of chronic joint pathologies such as rheumatoid arthritis and psoriatic arthritis, the increasing incidence of gout makes it a more palatable disease for novel drug discovery programs. This fact, associated with novel insights into the molecular mechanisms activated by the urate crystal deposition, is at the basis of new therapeutics under clinical development for gout, a valid example being the effective targeting of the proinflammatory cytokine interleukin-1. Here we briefly review the current status of antigout drug development and propose another target; our focus is on melanocortin receptor agonists as novel therapeutics for gout and inflammatory arthritides, a prototype of which, the adrenocorticotropic hormone, is already used in clinical settings. Inflammation (dpeaa)DE-He213 Macrophage (dpeaa)DE-He213 Animal models (dpeaa)DE-He213 Anti-inflammatory therapeutics (dpeaa)DE-He213 G-protein–coupled receptor (dpeaa)DE-He213 Drug discovery (dpeaa)DE-He213 Gout (dpeaa)DE-He213 Inflammatory arthritis (dpeaa)DE-He213 Interleukin-1 (dpeaa)DE-He213 Clinical development (dpeaa)DE-He213 Receptor agonists (dpeaa)DE-He213 Urate inflammation (dpeaa)DE-He213 ACTH (dpeaa)DE-He213 Melanocyte-stimulating hormone (dpeaa)DE-He213 Melanocortin receptor 3 (dpeaa)DE-He213 MC1 (dpeaa)DE-He213 MC3 (dpeaa)DE-He213 MC5 (dpeaa)DE-He213 Neutrophil recruitment (dpeaa)DE-He213 Patel, Hetal B. verfasserin aut Perretti, Mauro verfasserin aut Enthalten in Current rheumatology reports Philadelphia, Pa. : Current Science Inc., 1999 13(2011), 2 vom: 18. Jan., Seite 138-145 (DE-627)357168445 (DE-600)2094184-5 1534-6307 nnns volume:13 year:2011 number:2 day:18 month:01 pages:138-145 https://dx.doi.org/10.1007/s11926-011-0163-0 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 44.83 ASE AR 13 2011 2 18 01 138-145 |
spelling |
10.1007/s11926-011-0163-0 doi (DE-627)SPR023032227 (SPR)s11926-011-0163-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.83 bkl Montero-Melendez, Trinidad verfasserin aut Role of Melanocortin Receptors in the Regulation of Gouty Inflammation 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Gouty arthritis is a form of acute joint inflammation provoked by joint deposition of urate crystals. Although this acute pathology resolves after a few days, the marked degree of inflammation in the joint and—possibly more important to the patient—the excruciating pain it causes require proper therapeutic management. Often deemed a “poor sibling” of chronic joint pathologies such as rheumatoid arthritis and psoriatic arthritis, the increasing incidence of gout makes it a more palatable disease for novel drug discovery programs. This fact, associated with novel insights into the molecular mechanisms activated by the urate crystal deposition, is at the basis of new therapeutics under clinical development for gout, a valid example being the effective targeting of the proinflammatory cytokine interleukin-1. Here we briefly review the current status of antigout drug development and propose another target; our focus is on melanocortin receptor agonists as novel therapeutics for gout and inflammatory arthritides, a prototype of which, the adrenocorticotropic hormone, is already used in clinical settings. Inflammation (dpeaa)DE-He213 Macrophage (dpeaa)DE-He213 Animal models (dpeaa)DE-He213 Anti-inflammatory therapeutics (dpeaa)DE-He213 G-protein–coupled receptor (dpeaa)DE-He213 Drug discovery (dpeaa)DE-He213 Gout (dpeaa)DE-He213 Inflammatory arthritis (dpeaa)DE-He213 Interleukin-1 (dpeaa)DE-He213 Clinical development (dpeaa)DE-He213 Receptor agonists (dpeaa)DE-He213 Urate inflammation (dpeaa)DE-He213 ACTH (dpeaa)DE-He213 Melanocyte-stimulating hormone (dpeaa)DE-He213 Melanocortin receptor 3 (dpeaa)DE-He213 MC1 (dpeaa)DE-He213 MC3 (dpeaa)DE-He213 MC5 (dpeaa)DE-He213 Neutrophil recruitment (dpeaa)DE-He213 Patel, Hetal B. verfasserin aut Perretti, Mauro verfasserin aut Enthalten in Current rheumatology reports Philadelphia, Pa. : Current Science Inc., 1999 13(2011), 2 vom: 18. Jan., Seite 138-145 (DE-627)357168445 (DE-600)2094184-5 1534-6307 nnns volume:13 year:2011 number:2 day:18 month:01 pages:138-145 https://dx.doi.org/10.1007/s11926-011-0163-0 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 44.83 ASE AR 13 2011 2 18 01 138-145 |
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10.1007/s11926-011-0163-0 doi (DE-627)SPR023032227 (SPR)s11926-011-0163-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.83 bkl Montero-Melendez, Trinidad verfasserin aut Role of Melanocortin Receptors in the Regulation of Gouty Inflammation 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Gouty arthritis is a form of acute joint inflammation provoked by joint deposition of urate crystals. Although this acute pathology resolves after a few days, the marked degree of inflammation in the joint and—possibly more important to the patient—the excruciating pain it causes require proper therapeutic management. Often deemed a “poor sibling” of chronic joint pathologies such as rheumatoid arthritis and psoriatic arthritis, the increasing incidence of gout makes it a more palatable disease for novel drug discovery programs. This fact, associated with novel insights into the molecular mechanisms activated by the urate crystal deposition, is at the basis of new therapeutics under clinical development for gout, a valid example being the effective targeting of the proinflammatory cytokine interleukin-1. Here we briefly review the current status of antigout drug development and propose another target; our focus is on melanocortin receptor agonists as novel therapeutics for gout and inflammatory arthritides, a prototype of which, the adrenocorticotropic hormone, is already used in clinical settings. Inflammation (dpeaa)DE-He213 Macrophage (dpeaa)DE-He213 Animal models (dpeaa)DE-He213 Anti-inflammatory therapeutics (dpeaa)DE-He213 G-protein–coupled receptor (dpeaa)DE-He213 Drug discovery (dpeaa)DE-He213 Gout (dpeaa)DE-He213 Inflammatory arthritis (dpeaa)DE-He213 Interleukin-1 (dpeaa)DE-He213 Clinical development (dpeaa)DE-He213 Receptor agonists (dpeaa)DE-He213 Urate inflammation (dpeaa)DE-He213 ACTH (dpeaa)DE-He213 Melanocyte-stimulating hormone (dpeaa)DE-He213 Melanocortin receptor 3 (dpeaa)DE-He213 MC1 (dpeaa)DE-He213 MC3 (dpeaa)DE-He213 MC5 (dpeaa)DE-He213 Neutrophil recruitment (dpeaa)DE-He213 Patel, Hetal B. verfasserin aut Perretti, Mauro verfasserin aut Enthalten in Current rheumatology reports Philadelphia, Pa. : Current Science Inc., 1999 13(2011), 2 vom: 18. Jan., Seite 138-145 (DE-627)357168445 (DE-600)2094184-5 1534-6307 nnns volume:13 year:2011 number:2 day:18 month:01 pages:138-145 https://dx.doi.org/10.1007/s11926-011-0163-0 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 44.83 ASE AR 13 2011 2 18 01 138-145 |
allfieldsGer |
10.1007/s11926-011-0163-0 doi (DE-627)SPR023032227 (SPR)s11926-011-0163-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.83 bkl Montero-Melendez, Trinidad verfasserin aut Role of Melanocortin Receptors in the Regulation of Gouty Inflammation 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Gouty arthritis is a form of acute joint inflammation provoked by joint deposition of urate crystals. Although this acute pathology resolves after a few days, the marked degree of inflammation in the joint and—possibly more important to the patient—the excruciating pain it causes require proper therapeutic management. Often deemed a “poor sibling” of chronic joint pathologies such as rheumatoid arthritis and psoriatic arthritis, the increasing incidence of gout makes it a more palatable disease for novel drug discovery programs. This fact, associated with novel insights into the molecular mechanisms activated by the urate crystal deposition, is at the basis of new therapeutics under clinical development for gout, a valid example being the effective targeting of the proinflammatory cytokine interleukin-1. Here we briefly review the current status of antigout drug development and propose another target; our focus is on melanocortin receptor agonists as novel therapeutics for gout and inflammatory arthritides, a prototype of which, the adrenocorticotropic hormone, is already used in clinical settings. Inflammation (dpeaa)DE-He213 Macrophage (dpeaa)DE-He213 Animal models (dpeaa)DE-He213 Anti-inflammatory therapeutics (dpeaa)DE-He213 G-protein–coupled receptor (dpeaa)DE-He213 Drug discovery (dpeaa)DE-He213 Gout (dpeaa)DE-He213 Inflammatory arthritis (dpeaa)DE-He213 Interleukin-1 (dpeaa)DE-He213 Clinical development (dpeaa)DE-He213 Receptor agonists (dpeaa)DE-He213 Urate inflammation (dpeaa)DE-He213 ACTH (dpeaa)DE-He213 Melanocyte-stimulating hormone (dpeaa)DE-He213 Melanocortin receptor 3 (dpeaa)DE-He213 MC1 (dpeaa)DE-He213 MC3 (dpeaa)DE-He213 MC5 (dpeaa)DE-He213 Neutrophil recruitment (dpeaa)DE-He213 Patel, Hetal B. verfasserin aut Perretti, Mauro verfasserin aut Enthalten in Current rheumatology reports Philadelphia, Pa. : Current Science Inc., 1999 13(2011), 2 vom: 18. Jan., Seite 138-145 (DE-627)357168445 (DE-600)2094184-5 1534-6307 nnns volume:13 year:2011 number:2 day:18 month:01 pages:138-145 https://dx.doi.org/10.1007/s11926-011-0163-0 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 44.83 ASE AR 13 2011 2 18 01 138-145 |
allfieldsSound |
10.1007/s11926-011-0163-0 doi (DE-627)SPR023032227 (SPR)s11926-011-0163-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.83 bkl Montero-Melendez, Trinidad verfasserin aut Role of Melanocortin Receptors in the Regulation of Gouty Inflammation 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Gouty arthritis is a form of acute joint inflammation provoked by joint deposition of urate crystals. Although this acute pathology resolves after a few days, the marked degree of inflammation in the joint and—possibly more important to the patient—the excruciating pain it causes require proper therapeutic management. Often deemed a “poor sibling” of chronic joint pathologies such as rheumatoid arthritis and psoriatic arthritis, the increasing incidence of gout makes it a more palatable disease for novel drug discovery programs. This fact, associated with novel insights into the molecular mechanisms activated by the urate crystal deposition, is at the basis of new therapeutics under clinical development for gout, a valid example being the effective targeting of the proinflammatory cytokine interleukin-1. Here we briefly review the current status of antigout drug development and propose another target; our focus is on melanocortin receptor agonists as novel therapeutics for gout and inflammatory arthritides, a prototype of which, the adrenocorticotropic hormone, is already used in clinical settings. Inflammation (dpeaa)DE-He213 Macrophage (dpeaa)DE-He213 Animal models (dpeaa)DE-He213 Anti-inflammatory therapeutics (dpeaa)DE-He213 G-protein–coupled receptor (dpeaa)DE-He213 Drug discovery (dpeaa)DE-He213 Gout (dpeaa)DE-He213 Inflammatory arthritis (dpeaa)DE-He213 Interleukin-1 (dpeaa)DE-He213 Clinical development (dpeaa)DE-He213 Receptor agonists (dpeaa)DE-He213 Urate inflammation (dpeaa)DE-He213 ACTH (dpeaa)DE-He213 Melanocyte-stimulating hormone (dpeaa)DE-He213 Melanocortin receptor 3 (dpeaa)DE-He213 MC1 (dpeaa)DE-He213 MC3 (dpeaa)DE-He213 MC5 (dpeaa)DE-He213 Neutrophil recruitment (dpeaa)DE-He213 Patel, Hetal B. verfasserin aut Perretti, Mauro verfasserin aut Enthalten in Current rheumatology reports Philadelphia, Pa. : Current Science Inc., 1999 13(2011), 2 vom: 18. Jan., Seite 138-145 (DE-627)357168445 (DE-600)2094184-5 1534-6307 nnns volume:13 year:2011 number:2 day:18 month:01 pages:138-145 https://dx.doi.org/10.1007/s11926-011-0163-0 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 44.83 ASE AR 13 2011 2 18 01 138-145 |
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Enthalten in Current rheumatology reports 13(2011), 2 vom: 18. Jan., Seite 138-145 volume:13 year:2011 number:2 day:18 month:01 pages:138-145 |
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Enthalten in Current rheumatology reports 13(2011), 2 vom: 18. Jan., Seite 138-145 volume:13 year:2011 number:2 day:18 month:01 pages:138-145 |
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Inflammation Macrophage Animal models Anti-inflammatory therapeutics G-protein–coupled receptor Drug discovery Gout Inflammatory arthritis Interleukin-1 Clinical development Receptor agonists Urate inflammation ACTH Melanocyte-stimulating hormone Melanocortin receptor 3 MC1 MC3 MC5 Neutrophil recruitment |
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Current rheumatology reports |
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Montero-Melendez, Trinidad @@aut@@ Patel, Hetal B. @@aut@@ Perretti, Mauro @@aut@@ |
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2011-01-18T00:00:00Z |
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Although this acute pathology resolves after a few days, the marked degree of inflammation in the joint and—possibly more important to the patient—the excruciating pain it causes require proper therapeutic management. Often deemed a “poor sibling” of chronic joint pathologies such as rheumatoid arthritis and psoriatic arthritis, the increasing incidence of gout makes it a more palatable disease for novel drug discovery programs. This fact, associated with novel insights into the molecular mechanisms activated by the urate crystal deposition, is at the basis of new therapeutics under clinical development for gout, a valid example being the effective targeting of the proinflammatory cytokine interleukin-1. 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|
author |
Montero-Melendez, Trinidad |
spellingShingle |
Montero-Melendez, Trinidad ddc 610 bkl 44.83 misc Inflammation misc Macrophage misc Animal models misc Anti-inflammatory therapeutics misc G-protein–coupled receptor misc Drug discovery misc Gout misc Inflammatory arthritis misc Interleukin-1 misc Clinical development misc Receptor agonists misc Urate inflammation misc ACTH misc Melanocyte-stimulating hormone misc Melanocortin receptor 3 misc MC1 misc MC3 misc MC5 misc Neutrophil recruitment Role of Melanocortin Receptors in the Regulation of Gouty Inflammation |
authorStr |
Montero-Melendez, Trinidad |
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@@773@@(DE-627)357168445 |
format |
electronic Article |
dewey-ones |
610 - Medicine & health |
delete_txt_mv |
keep |
author_role |
aut aut aut |
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springer |
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true |
illustrated |
Not Illustrated |
issn |
1534-6307 |
topic_title |
610 ASE 44.83 bkl Role of Melanocortin Receptors in the Regulation of Gouty Inflammation Inflammation (dpeaa)DE-He213 Macrophage (dpeaa)DE-He213 Animal models (dpeaa)DE-He213 Anti-inflammatory therapeutics (dpeaa)DE-He213 G-protein–coupled receptor (dpeaa)DE-He213 Drug discovery (dpeaa)DE-He213 Gout (dpeaa)DE-He213 Inflammatory arthritis (dpeaa)DE-He213 Interleukin-1 (dpeaa)DE-He213 Clinical development (dpeaa)DE-He213 Receptor agonists (dpeaa)DE-He213 Urate inflammation (dpeaa)DE-He213 ACTH (dpeaa)DE-He213 Melanocyte-stimulating hormone (dpeaa)DE-He213 Melanocortin receptor 3 (dpeaa)DE-He213 MC1 (dpeaa)DE-He213 MC3 (dpeaa)DE-He213 MC5 (dpeaa)DE-He213 Neutrophil recruitment (dpeaa)DE-He213 |
topic |
ddc 610 bkl 44.83 misc Inflammation misc Macrophage misc Animal models misc Anti-inflammatory therapeutics misc G-protein–coupled receptor misc Drug discovery misc Gout misc Inflammatory arthritis misc Interleukin-1 misc Clinical development misc Receptor agonists misc Urate inflammation misc ACTH misc Melanocyte-stimulating hormone misc Melanocortin receptor 3 misc MC1 misc MC3 misc MC5 misc Neutrophil recruitment |
topic_unstemmed |
ddc 610 bkl 44.83 misc Inflammation misc Macrophage misc Animal models misc Anti-inflammatory therapeutics misc G-protein–coupled receptor misc Drug discovery misc Gout misc Inflammatory arthritis misc Interleukin-1 misc Clinical development misc Receptor agonists misc Urate inflammation misc ACTH misc Melanocyte-stimulating hormone misc Melanocortin receptor 3 misc MC1 misc MC3 misc MC5 misc Neutrophil recruitment |
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ddc 610 bkl 44.83 misc Inflammation misc Macrophage misc Animal models misc Anti-inflammatory therapeutics misc G-protein–coupled receptor misc Drug discovery misc Gout misc Inflammatory arthritis misc Interleukin-1 misc Clinical development misc Receptor agonists misc Urate inflammation misc ACTH misc Melanocyte-stimulating hormone misc Melanocortin receptor 3 misc MC1 misc MC3 misc MC5 misc Neutrophil recruitment |
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Role of Melanocortin Receptors in the Regulation of Gouty Inflammation |
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Role of Melanocortin Receptors in the Regulation of Gouty Inflammation |
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role of melanocortin receptors in the regulation of gouty inflammation |
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Role of Melanocortin Receptors in the Regulation of Gouty Inflammation |
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Abstract Gouty arthritis is a form of acute joint inflammation provoked by joint deposition of urate crystals. Although this acute pathology resolves after a few days, the marked degree of inflammation in the joint and—possibly more important to the patient—the excruciating pain it causes require proper therapeutic management. Often deemed a “poor sibling” of chronic joint pathologies such as rheumatoid arthritis and psoriatic arthritis, the increasing incidence of gout makes it a more palatable disease for novel drug discovery programs. This fact, associated with novel insights into the molecular mechanisms activated by the urate crystal deposition, is at the basis of new therapeutics under clinical development for gout, a valid example being the effective targeting of the proinflammatory cytokine interleukin-1. Here we briefly review the current status of antigout drug development and propose another target; our focus is on melanocortin receptor agonists as novel therapeutics for gout and inflammatory arthritides, a prototype of which, the adrenocorticotropic hormone, is already used in clinical settings. |
abstractGer |
Abstract Gouty arthritis is a form of acute joint inflammation provoked by joint deposition of urate crystals. Although this acute pathology resolves after a few days, the marked degree of inflammation in the joint and—possibly more important to the patient—the excruciating pain it causes require proper therapeutic management. Often deemed a “poor sibling” of chronic joint pathologies such as rheumatoid arthritis and psoriatic arthritis, the increasing incidence of gout makes it a more palatable disease for novel drug discovery programs. This fact, associated with novel insights into the molecular mechanisms activated by the urate crystal deposition, is at the basis of new therapeutics under clinical development for gout, a valid example being the effective targeting of the proinflammatory cytokine interleukin-1. Here we briefly review the current status of antigout drug development and propose another target; our focus is on melanocortin receptor agonists as novel therapeutics for gout and inflammatory arthritides, a prototype of which, the adrenocorticotropic hormone, is already used in clinical settings. |
abstract_unstemmed |
Abstract Gouty arthritis is a form of acute joint inflammation provoked by joint deposition of urate crystals. Although this acute pathology resolves after a few days, the marked degree of inflammation in the joint and—possibly more important to the patient—the excruciating pain it causes require proper therapeutic management. Often deemed a “poor sibling” of chronic joint pathologies such as rheumatoid arthritis and psoriatic arthritis, the increasing incidence of gout makes it a more palatable disease for novel drug discovery programs. This fact, associated with novel insights into the molecular mechanisms activated by the urate crystal deposition, is at the basis of new therapeutics under clinical development for gout, a valid example being the effective targeting of the proinflammatory cytokine interleukin-1. Here we briefly review the current status of antigout drug development and propose another target; our focus is on melanocortin receptor agonists as novel therapeutics for gout and inflammatory arthritides, a prototype of which, the adrenocorticotropic hormone, is already used in clinical settings. |
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Role of Melanocortin Receptors in the Regulation of Gouty Inflammation |
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|
score |
7.400262 |