Hydrogen Sulfide: A Therapeutic Candidate for Fibrotic Disease?

Fibrotic diseases including chronic kidney disease, liver cirrhosis, idiopathic pulmonary fibrosis, and chronic disease account for 45% mortality in the developed countries and pose a great threat to the global health. Many great targets and molecules have been reported to be involved in the initiat...
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Autor*in:	Kai Song [verfasserIn] Qian Li [verfasserIn] Xiao-Ya Yin [verfasserIn] Ying Lu [verfasserIn] Chun-Feng Liu [verfasserIn] Li-Fang Hu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2015

Übergeordnetes Werk:	In: Oxidative Medicine and Cellular Longevity - Hindawi Limited, 2011, (2015)
Übergeordnetes Werk:	year:2015

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1155/2015/458720

Katalog-ID:	DOAJ012781649

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520			\|a Fibrotic diseases including chronic kidney disease, liver cirrhosis, idiopathic pulmonary fibrosis, and chronic disease account for 45% mortality in the developed countries and pose a great threat to the global health. Many great targets and molecules have been reported to be involved in the initiation and/or progression of fibrosis, among which inflammation and oxidative stress are well-recognized modulation targets. Hydrogen sulfide (H2S) is the third gasotransmitter with potent properties in inhibiting inflammation and oxidative stress in various organs. Recent evidence suggests that plasma H2S level is decreased in various animal models of fibrotic diseases and supplement of exogenous H2S is able to ameliorate fibrosis in the kidney, lung, liver, and heart. This leads us to propose that modulation of H2S production may represent a promising therapeutic venue for the treatment of a variety of fibrotic diseases. Here, we summarize and discuss the current data on the role and underlying mechanisms of H2S in fibrosis diseases related to heart, liver, kidney, and other organs.
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allfields	10.1155/2015/458720 doi (DE-627)DOAJ012781649 (DE-599)DOAJ6551a07092d9406aa7a1d50b65025cd3 DE-627 ger DE-627 rakwb eng QH573-671 Kai Song verfasserin aut Hydrogen Sulfide: A Therapeutic Candidate for Fibrotic Disease? 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Fibrotic diseases including chronic kidney disease, liver cirrhosis, idiopathic pulmonary fibrosis, and chronic disease account for 45% mortality in the developed countries and pose a great threat to the global health. Many great targets and molecules have been reported to be involved in the initiation and/or progression of fibrosis, among which inflammation and oxidative stress are well-recognized modulation targets. Hydrogen sulfide (H2S) is the third gasotransmitter with potent properties in inhibiting inflammation and oxidative stress in various organs. Recent evidence suggests that plasma H2S level is decreased in various animal models of fibrotic diseases and supplement of exogenous H2S is able to ameliorate fibrosis in the kidney, lung, liver, and heart. This leads us to propose that modulation of H2S production may represent a promising therapeutic venue for the treatment of a variety of fibrotic diseases. Here, we summarize and discuss the current data on the role and underlying mechanisms of H2S in fibrosis diseases related to heart, liver, kidney, and other organs. Cytology Qian Li verfasserin aut Xiao-Ya Yin verfasserin aut Ying Lu verfasserin aut Chun-Feng Liu verfasserin aut Li-Fang Hu verfasserin aut In Oxidative Medicine and Cellular Longevity Hindawi Limited, 2011 (2015) (DE-627)582019079 (DE-600)2455981-7 19420994 nnns year:2015 https://doi.org/10.1155/2015/458720 kostenfrei https://doaj.org/article/6551a07092d9406aa7a1d50b65025cd3 kostenfrei http://dx.doi.org/10.1155/2015/458720 kostenfrei https://doaj.org/toc/1942-0900 Journal toc kostenfrei https://doaj.org/toc/1942-0994 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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_4367 GBV_ILN_4700 AR 2015
spelling	10.1155/2015/458720 doi (DE-627)DOAJ012781649 (DE-599)DOAJ6551a07092d9406aa7a1d50b65025cd3 DE-627 ger DE-627 rakwb eng QH573-671 Kai Song verfasserin aut Hydrogen Sulfide: A Therapeutic Candidate for Fibrotic Disease? 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Fibrotic diseases including chronic kidney disease, liver cirrhosis, idiopathic pulmonary fibrosis, and chronic disease account for 45% mortality in the developed countries and pose a great threat to the global health. Many great targets and molecules have been reported to be involved in the initiation and/or progression of fibrosis, among which inflammation and oxidative stress are well-recognized modulation targets. Hydrogen sulfide (H2S) is the third gasotransmitter with potent properties in inhibiting inflammation and oxidative stress in various organs. Recent evidence suggests that plasma H2S level is decreased in various animal models of fibrotic diseases and supplement of exogenous H2S is able to ameliorate fibrosis in the kidney, lung, liver, and heart. This leads us to propose that modulation of H2S production may represent a promising therapeutic venue for the treatment of a variety of fibrotic diseases. Here, we summarize and discuss the current data on the role and underlying mechanisms of H2S in fibrosis diseases related to heart, liver, kidney, and other organs. Cytology Qian Li verfasserin aut Xiao-Ya Yin verfasserin aut Ying Lu verfasserin aut Chun-Feng Liu verfasserin aut Li-Fang Hu verfasserin aut In Oxidative Medicine and Cellular Longevity Hindawi Limited, 2011 (2015) (DE-627)582019079 (DE-600)2455981-7 19420994 nnns year:2015 https://doi.org/10.1155/2015/458720 kostenfrei https://doaj.org/article/6551a07092d9406aa7a1d50b65025cd3 kostenfrei http://dx.doi.org/10.1155/2015/458720 kostenfrei https://doaj.org/toc/1942-0900 Journal toc kostenfrei https://doaj.org/toc/1942-0994 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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_4367 GBV_ILN_4700 AR 2015
allfields_unstemmed	10.1155/2015/458720 doi (DE-627)DOAJ012781649 (DE-599)DOAJ6551a07092d9406aa7a1d50b65025cd3 DE-627 ger DE-627 rakwb eng QH573-671 Kai Song verfasserin aut Hydrogen Sulfide: A Therapeutic Candidate for Fibrotic Disease? 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Fibrotic diseases including chronic kidney disease, liver cirrhosis, idiopathic pulmonary fibrosis, and chronic disease account for 45% mortality in the developed countries and pose a great threat to the global health. Many great targets and molecules have been reported to be involved in the initiation and/or progression of fibrosis, among which inflammation and oxidative stress are well-recognized modulation targets. Hydrogen sulfide (H2S) is the third gasotransmitter with potent properties in inhibiting inflammation and oxidative stress in various organs. Recent evidence suggests that plasma H2S level is decreased in various animal models of fibrotic diseases and supplement of exogenous H2S is able to ameliorate fibrosis in the kidney, lung, liver, and heart. This leads us to propose that modulation of H2S production may represent a promising therapeutic venue for the treatment of a variety of fibrotic diseases. Here, we summarize and discuss the current data on the role and underlying mechanisms of H2S in fibrosis diseases related to heart, liver, kidney, and other organs. Cytology Qian Li verfasserin aut Xiao-Ya Yin verfasserin aut Ying Lu verfasserin aut Chun-Feng Liu verfasserin aut Li-Fang Hu verfasserin aut In Oxidative Medicine and Cellular Longevity Hindawi Limited, 2011 (2015) (DE-627)582019079 (DE-600)2455981-7 19420994 nnns year:2015 https://doi.org/10.1155/2015/458720 kostenfrei https://doaj.org/article/6551a07092d9406aa7a1d50b65025cd3 kostenfrei http://dx.doi.org/10.1155/2015/458720 kostenfrei https://doaj.org/toc/1942-0900 Journal toc kostenfrei https://doaj.org/toc/1942-0994 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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_4367 GBV_ILN_4700 AR 2015
allfieldsGer	10.1155/2015/458720 doi (DE-627)DOAJ012781649 (DE-599)DOAJ6551a07092d9406aa7a1d50b65025cd3 DE-627 ger DE-627 rakwb eng QH573-671 Kai Song verfasserin aut Hydrogen Sulfide: A Therapeutic Candidate for Fibrotic Disease? 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Fibrotic diseases including chronic kidney disease, liver cirrhosis, idiopathic pulmonary fibrosis, and chronic disease account for 45% mortality in the developed countries and pose a great threat to the global health. Many great targets and molecules have been reported to be involved in the initiation and/or progression of fibrosis, among which inflammation and oxidative stress are well-recognized modulation targets. Hydrogen sulfide (H2S) is the third gasotransmitter with potent properties in inhibiting inflammation and oxidative stress in various organs. Recent evidence suggests that plasma H2S level is decreased in various animal models of fibrotic diseases and supplement of exogenous H2S is able to ameliorate fibrosis in the kidney, lung, liver, and heart. This leads us to propose that modulation of H2S production may represent a promising therapeutic venue for the treatment of a variety of fibrotic diseases. Here, we summarize and discuss the current data on the role and underlying mechanisms of H2S in fibrosis diseases related to heart, liver, kidney, and other organs. Cytology Qian Li verfasserin aut Xiao-Ya Yin verfasserin aut Ying Lu verfasserin aut Chun-Feng Liu verfasserin aut Li-Fang Hu verfasserin aut In Oxidative Medicine and Cellular Longevity Hindawi Limited, 2011 (2015) (DE-627)582019079 (DE-600)2455981-7 19420994 nnns year:2015 https://doi.org/10.1155/2015/458720 kostenfrei https://doaj.org/article/6551a07092d9406aa7a1d50b65025cd3 kostenfrei http://dx.doi.org/10.1155/2015/458720 kostenfrei https://doaj.org/toc/1942-0900 Journal toc kostenfrei https://doaj.org/toc/1942-0994 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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_4367 GBV_ILN_4700 AR 2015
allfieldsSound	10.1155/2015/458720 doi (DE-627)DOAJ012781649 (DE-599)DOAJ6551a07092d9406aa7a1d50b65025cd3 DE-627 ger DE-627 rakwb eng QH573-671 Kai Song verfasserin aut Hydrogen Sulfide: A Therapeutic Candidate for Fibrotic Disease? 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Fibrotic diseases including chronic kidney disease, liver cirrhosis, idiopathic pulmonary fibrosis, and chronic disease account for 45% mortality in the developed countries and pose a great threat to the global health. Many great targets and molecules have been reported to be involved in the initiation and/or progression of fibrosis, among which inflammation and oxidative stress are well-recognized modulation targets. Hydrogen sulfide (H2S) is the third gasotransmitter with potent properties in inhibiting inflammation and oxidative stress in various organs. Recent evidence suggests that plasma H2S level is decreased in various animal models of fibrotic diseases and supplement of exogenous H2S is able to ameliorate fibrosis in the kidney, lung, liver, and heart. This leads us to propose that modulation of H2S production may represent a promising therapeutic venue for the treatment of a variety of fibrotic diseases. Here, we summarize and discuss the current data on the role and underlying mechanisms of H2S in fibrosis diseases related to heart, liver, kidney, and other organs. Cytology Qian Li verfasserin aut Xiao-Ya Yin verfasserin aut Ying Lu verfasserin aut Chun-Feng Liu verfasserin aut Li-Fang Hu verfasserin aut In Oxidative Medicine and Cellular Longevity Hindawi Limited, 2011 (2015) (DE-627)582019079 (DE-600)2455981-7 19420994 nnns year:2015 https://doi.org/10.1155/2015/458720 kostenfrei https://doaj.org/article/6551a07092d9406aa7a1d50b65025cd3 kostenfrei http://dx.doi.org/10.1155/2015/458720 kostenfrei https://doaj.org/toc/1942-0900 Journal toc kostenfrei https://doaj.org/toc/1942-0994 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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_4367 GBV_ILN_4700 AR 2015
language	English
source	In Oxidative Medicine and Cellular Longevity (2015) year:2015
sourceStr	In Oxidative Medicine and Cellular Longevity (2015) year:2015
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Cytology
isfreeaccess_bool	true
container_title	Oxidative Medicine and Cellular Longevity
authorswithroles_txt_mv	Kai Song @@aut@@ Qian Li @@aut@@ Xiao-Ya Yin @@aut@@ Ying Lu @@aut@@ Chun-Feng Liu @@aut@@ Li-Fang Hu @@aut@@
publishDateDaySort_date	2015-01-01T00:00:00Z
hierarchy_top_id	582019079
id	DOAJ012781649
language_de	englisch
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topic_title	QH573-671 Hydrogen Sulfide: A Therapeutic Candidate for Fibrotic Disease?
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title	Hydrogen Sulfide: A Therapeutic Candidate for Fibrotic Disease?
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title_full	Hydrogen Sulfide: A Therapeutic Candidate for Fibrotic Disease?
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title_sort	hydrogen sulfide: a therapeutic candidate for fibrotic disease?
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title_auth	Hydrogen Sulfide: A Therapeutic Candidate for Fibrotic Disease?
abstract	Fibrotic diseases including chronic kidney disease, liver cirrhosis, idiopathic pulmonary fibrosis, and chronic disease account for 45% mortality in the developed countries and pose a great threat to the global health. Many great targets and molecules have been reported to be involved in the initiation and/or progression of fibrosis, among which inflammation and oxidative stress are well-recognized modulation targets. Hydrogen sulfide (H2S) is the third gasotransmitter with potent properties in inhibiting inflammation and oxidative stress in various organs. Recent evidence suggests that plasma H2S level is decreased in various animal models of fibrotic diseases and supplement of exogenous H2S is able to ameliorate fibrosis in the kidney, lung, liver, and heart. This leads us to propose that modulation of H2S production may represent a promising therapeutic venue for the treatment of a variety of fibrotic diseases. Here, we summarize and discuss the current data on the role and underlying mechanisms of H2S in fibrosis diseases related to heart, liver, kidney, and other organs.
abstractGer	Fibrotic diseases including chronic kidney disease, liver cirrhosis, idiopathic pulmonary fibrosis, and chronic disease account for 45% mortality in the developed countries and pose a great threat to the global health. Many great targets and molecules have been reported to be involved in the initiation and/or progression of fibrosis, among which inflammation and oxidative stress are well-recognized modulation targets. Hydrogen sulfide (H2S) is the third gasotransmitter with potent properties in inhibiting inflammation and oxidative stress in various organs. Recent evidence suggests that plasma H2S level is decreased in various animal models of fibrotic diseases and supplement of exogenous H2S is able to ameliorate fibrosis in the kidney, lung, liver, and heart. This leads us to propose that modulation of H2S production may represent a promising therapeutic venue for the treatment of a variety of fibrotic diseases. Here, we summarize and discuss the current data on the role and underlying mechanisms of H2S in fibrosis diseases related to heart, liver, kidney, and other organs.
abstract_unstemmed	Fibrotic diseases including chronic kidney disease, liver cirrhosis, idiopathic pulmonary fibrosis, and chronic disease account for 45% mortality in the developed countries and pose a great threat to the global health. Many great targets and molecules have been reported to be involved in the initiation and/or progression of fibrosis, among which inflammation and oxidative stress are well-recognized modulation targets. Hydrogen sulfide (H2S) is the third gasotransmitter with potent properties in inhibiting inflammation and oxidative stress in various organs. Recent evidence suggests that plasma H2S level is decreased in various animal models of fibrotic diseases and supplement of exogenous H2S is able to ameliorate fibrosis in the kidney, lung, liver, and heart. This leads us to propose that modulation of H2S production may represent a promising therapeutic venue for the treatment of a variety of fibrotic diseases. Here, we summarize and discuss the current data on the role and underlying mechanisms of H2S in fibrosis diseases related to heart, liver, kidney, and other organs.
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title_short	Hydrogen Sulfide: A Therapeutic Candidate for Fibrotic Disease?
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