Carboxyl‐Terminal Modulator Protein Ameliorates Pathological Cardiac Hypertrophy by Suppressing the Protein Kinase B Signaling Pathway

Background Carboxyl‐terminal modulator protein (CTMP) has been implicated in cancer, brain injury, and obesity. However, the role of CTMP in pathological cardiac hypertrophy has not been identified. Methods and Results In this study, decreased expression of CTMP was observed in both human failing he...
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Autor*in:	Xiaoxiong Liu [verfasserIn] Qin Yang [verfasserIn] Li‐Hua Zhu [verfasserIn] Jia Liu [verfasserIn] Ke‐Qiong Deng [verfasserIn] Xue‐Yong Zhu [verfasserIn] Ye Liu [verfasserIn] Jun Gong [verfasserIn] Peng Zhang [verfasserIn] Shuyan Li [verfasserIn] Hao Xia [verfasserIn] Zhi‐Gang She [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	angiotensin II aortic banding carboxyl‐terminal modulator protein pathological cardiac hypertrophy signal transduction

Übergeordnetes Werk:	In: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease - Wiley, 2012, 7(2018), 13
Übergeordnetes Werk:	volume:7 ; year:2018 ; number:13

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1161/JAHA.118.008654

Katalog-ID:	DOAJ007565224

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520			\|a Background Carboxyl‐terminal modulator protein (CTMP) has been implicated in cancer, brain injury, and obesity. However, the role of CTMP in pathological cardiac hypertrophy has not been identified. Methods and Results In this study, decreased expression of CTMP was observed in both human failing hearts and murine hypertrophied hearts. To further explore the potential involvement of CTMP in pathological cardiac hypertrophy, cardiac‐specific CTMP knockout and overexpression mice were generated. In vivo experiments revealed that CTMP deficiency exacerbated the cardiac hypertrophy, fibrosis, and function induced by pressure overload, whereas CTMP overexpression alleviated the response to hypertrophic stimuli. Consistent with the in vivo results, adenovirus‐mediated gain‐of‐function or loss‐of‐function experiments showed that CTMP also exerted a protective effect against hypertrophic responses to angiotensin II in vitro. Mechanistically, CTMP ameliorated pathological cardiac hypertrophy through the blockade of the protein kinase B signaling pathway. Moreover, inhibition of protein kinase B activation with LY294002 rescued the deteriorated effect in aortic banding–treated cardiac‐specific CTMP knockout mice. Conclusions Taken together, these findings imply, for the first time, that increasing the cardiac expression of CTMP may be a novel therapeutic strategy for pathological cardiac hypertrophy.
650		4	\|a angiotensin II
650		4	\|a aortic banding
650		4	\|a carboxyl‐terminal modulator protein
650		4	\|a pathological cardiac hypertrophy
650		4	\|a signal transduction
653		0	\|a Diseases of the circulatory (Cardiovascular) system
700	0		\|a Qin Yang \|e verfasserin \|4 aut
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700	0		\|a Ke‐Qiong Deng \|e verfasserin \|4 aut
700	0		\|a Xue‐Yong Zhu \|e verfasserin \|4 aut
700	0		\|a Ye Liu \|e verfasserin \|4 aut
700	0		\|a Jun Gong \|e verfasserin \|4 aut
700	0		\|a Peng Zhang \|e verfasserin \|4 aut
700	0		\|a Shuyan Li \|e verfasserin \|4 aut
700	0		\|a Hao Xia \|e verfasserin \|4 aut
700	0		\|a Zhi‐Gang She \|e verfasserin \|4 aut
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author_variant	x l xl q y qy l z lz j l jl k d kd x z xz y l yl j g jg p z pz s l sl h x hx z s zs
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allfields	10.1161/JAHA.118.008654 doi (DE-627)DOAJ007565224 (DE-599)DOAJ88882cacec304168b65de30be4e8ce31 DE-627 ger DE-627 rakwb eng RC666-701 Xiaoxiong Liu verfasserin aut Carboxyl‐Terminal Modulator Protein Ameliorates Pathological Cardiac Hypertrophy by Suppressing the Protein Kinase B Signaling Pathway 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Carboxyl‐terminal modulator protein (CTMP) has been implicated in cancer, brain injury, and obesity. However, the role of CTMP in pathological cardiac hypertrophy has not been identified. Methods and Results In this study, decreased expression of CTMP was observed in both human failing hearts and murine hypertrophied hearts. To further explore the potential involvement of CTMP in pathological cardiac hypertrophy, cardiac‐specific CTMP knockout and overexpression mice were generated. In vivo experiments revealed that CTMP deficiency exacerbated the cardiac hypertrophy, fibrosis, and function induced by pressure overload, whereas CTMP overexpression alleviated the response to hypertrophic stimuli. Consistent with the in vivo results, adenovirus‐mediated gain‐of‐function or loss‐of‐function experiments showed that CTMP also exerted a protective effect against hypertrophic responses to angiotensin II in vitro. Mechanistically, CTMP ameliorated pathological cardiac hypertrophy through the blockade of the protein kinase B signaling pathway. Moreover, inhibition of protein kinase B activation with LY294002 rescued the deteriorated effect in aortic banding–treated cardiac‐specific CTMP knockout mice. Conclusions Taken together, these findings imply, for the first time, that increasing the cardiac expression of CTMP may be a novel therapeutic strategy for pathological cardiac hypertrophy. angiotensin II aortic banding carboxyl‐terminal modulator protein pathological cardiac hypertrophy signal transduction Diseases of the circulatory (Cardiovascular) system Qin Yang verfasserin aut Li‐Hua Zhu verfasserin aut Jia Liu verfasserin aut Ke‐Qiong Deng verfasserin aut Xue‐Yong Zhu verfasserin aut Ye Liu verfasserin aut Jun Gong verfasserin aut Peng Zhang verfasserin aut Shuyan Li verfasserin aut Hao Xia verfasserin aut Zhi‐Gang She verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 7(2018), 13 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:7 year:2018 number:13 https://doi.org/10.1161/JAHA.118.008654 kostenfrei https://doaj.org/article/88882cacec304168b65de30be4e8ce31 kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.118.008654 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_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_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_2049 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_2336 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 7 2018 13
spelling	10.1161/JAHA.118.008654 doi (DE-627)DOAJ007565224 (DE-599)DOAJ88882cacec304168b65de30be4e8ce31 DE-627 ger DE-627 rakwb eng RC666-701 Xiaoxiong Liu verfasserin aut Carboxyl‐Terminal Modulator Protein Ameliorates Pathological Cardiac Hypertrophy by Suppressing the Protein Kinase B Signaling Pathway 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Carboxyl‐terminal modulator protein (CTMP) has been implicated in cancer, brain injury, and obesity. However, the role of CTMP in pathological cardiac hypertrophy has not been identified. Methods and Results In this study, decreased expression of CTMP was observed in both human failing hearts and murine hypertrophied hearts. To further explore the potential involvement of CTMP in pathological cardiac hypertrophy, cardiac‐specific CTMP knockout and overexpression mice were generated. In vivo experiments revealed that CTMP deficiency exacerbated the cardiac hypertrophy, fibrosis, and function induced by pressure overload, whereas CTMP overexpression alleviated the response to hypertrophic stimuli. Consistent with the in vivo results, adenovirus‐mediated gain‐of‐function or loss‐of‐function experiments showed that CTMP also exerted a protective effect against hypertrophic responses to angiotensin II in vitro. Mechanistically, CTMP ameliorated pathological cardiac hypertrophy through the blockade of the protein kinase B signaling pathway. Moreover, inhibition of protein kinase B activation with LY294002 rescued the deteriorated effect in aortic banding–treated cardiac‐specific CTMP knockout mice. Conclusions Taken together, these findings imply, for the first time, that increasing the cardiac expression of CTMP may be a novel therapeutic strategy for pathological cardiac hypertrophy. angiotensin II aortic banding carboxyl‐terminal modulator protein pathological cardiac hypertrophy signal transduction Diseases of the circulatory (Cardiovascular) system Qin Yang verfasserin aut Li‐Hua Zhu verfasserin aut Jia Liu verfasserin aut Ke‐Qiong Deng verfasserin aut Xue‐Yong Zhu verfasserin aut Ye Liu verfasserin aut Jun Gong verfasserin aut Peng Zhang verfasserin aut Shuyan Li verfasserin aut Hao Xia verfasserin aut Zhi‐Gang She verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 7(2018), 13 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:7 year:2018 number:13 https://doi.org/10.1161/JAHA.118.008654 kostenfrei https://doaj.org/article/88882cacec304168b65de30be4e8ce31 kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.118.008654 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_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_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_2049 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_2336 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 7 2018 13
allfields_unstemmed	10.1161/JAHA.118.008654 doi (DE-627)DOAJ007565224 (DE-599)DOAJ88882cacec304168b65de30be4e8ce31 DE-627 ger DE-627 rakwb eng RC666-701 Xiaoxiong Liu verfasserin aut Carboxyl‐Terminal Modulator Protein Ameliorates Pathological Cardiac Hypertrophy by Suppressing the Protein Kinase B Signaling Pathway 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Carboxyl‐terminal modulator protein (CTMP) has been implicated in cancer, brain injury, and obesity. However, the role of CTMP in pathological cardiac hypertrophy has not been identified. Methods and Results In this study, decreased expression of CTMP was observed in both human failing hearts and murine hypertrophied hearts. To further explore the potential involvement of CTMP in pathological cardiac hypertrophy, cardiac‐specific CTMP knockout and overexpression mice were generated. In vivo experiments revealed that CTMP deficiency exacerbated the cardiac hypertrophy, fibrosis, and function induced by pressure overload, whereas CTMP overexpression alleviated the response to hypertrophic stimuli. Consistent with the in vivo results, adenovirus‐mediated gain‐of‐function or loss‐of‐function experiments showed that CTMP also exerted a protective effect against hypertrophic responses to angiotensin II in vitro. Mechanistically, CTMP ameliorated pathological cardiac hypertrophy through the blockade of the protein kinase B signaling pathway. Moreover, inhibition of protein kinase B activation with LY294002 rescued the deteriorated effect in aortic banding–treated cardiac‐specific CTMP knockout mice. Conclusions Taken together, these findings imply, for the first time, that increasing the cardiac expression of CTMP may be a novel therapeutic strategy for pathological cardiac hypertrophy. angiotensin II aortic banding carboxyl‐terminal modulator protein pathological cardiac hypertrophy signal transduction Diseases of the circulatory (Cardiovascular) system Qin Yang verfasserin aut Li‐Hua Zhu verfasserin aut Jia Liu verfasserin aut Ke‐Qiong Deng verfasserin aut Xue‐Yong Zhu verfasserin aut Ye Liu verfasserin aut Jun Gong verfasserin aut Peng Zhang verfasserin aut Shuyan Li verfasserin aut Hao Xia verfasserin aut Zhi‐Gang She verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 7(2018), 13 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:7 year:2018 number:13 https://doi.org/10.1161/JAHA.118.008654 kostenfrei https://doaj.org/article/88882cacec304168b65de30be4e8ce31 kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.118.008654 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_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_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_2049 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_2336 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 7 2018 13
allfieldsGer	10.1161/JAHA.118.008654 doi (DE-627)DOAJ007565224 (DE-599)DOAJ88882cacec304168b65de30be4e8ce31 DE-627 ger DE-627 rakwb eng RC666-701 Xiaoxiong Liu verfasserin aut Carboxyl‐Terminal Modulator Protein Ameliorates Pathological Cardiac Hypertrophy by Suppressing the Protein Kinase B Signaling Pathway 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Carboxyl‐terminal modulator protein (CTMP) has been implicated in cancer, brain injury, and obesity. However, the role of CTMP in pathological cardiac hypertrophy has not been identified. Methods and Results In this study, decreased expression of CTMP was observed in both human failing hearts and murine hypertrophied hearts. To further explore the potential involvement of CTMP in pathological cardiac hypertrophy, cardiac‐specific CTMP knockout and overexpression mice were generated. In vivo experiments revealed that CTMP deficiency exacerbated the cardiac hypertrophy, fibrosis, and function induced by pressure overload, whereas CTMP overexpression alleviated the response to hypertrophic stimuli. Consistent with the in vivo results, adenovirus‐mediated gain‐of‐function or loss‐of‐function experiments showed that CTMP also exerted a protective effect against hypertrophic responses to angiotensin II in vitro. Mechanistically, CTMP ameliorated pathological cardiac hypertrophy through the blockade of the protein kinase B signaling pathway. Moreover, inhibition of protein kinase B activation with LY294002 rescued the deteriorated effect in aortic banding–treated cardiac‐specific CTMP knockout mice. Conclusions Taken together, these findings imply, for the first time, that increasing the cardiac expression of CTMP may be a novel therapeutic strategy for pathological cardiac hypertrophy. angiotensin II aortic banding carboxyl‐terminal modulator protein pathological cardiac hypertrophy signal transduction Diseases of the circulatory (Cardiovascular) system Qin Yang verfasserin aut Li‐Hua Zhu verfasserin aut Jia Liu verfasserin aut Ke‐Qiong Deng verfasserin aut Xue‐Yong Zhu verfasserin aut Ye Liu verfasserin aut Jun Gong verfasserin aut Peng Zhang verfasserin aut Shuyan Li verfasserin aut Hao Xia verfasserin aut Zhi‐Gang She verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 7(2018), 13 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:7 year:2018 number:13 https://doi.org/10.1161/JAHA.118.008654 kostenfrei https://doaj.org/article/88882cacec304168b65de30be4e8ce31 kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.118.008654 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_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_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_2049 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_2336 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 7 2018 13
allfieldsSound	10.1161/JAHA.118.008654 doi (DE-627)DOAJ007565224 (DE-599)DOAJ88882cacec304168b65de30be4e8ce31 DE-627 ger DE-627 rakwb eng RC666-701 Xiaoxiong Liu verfasserin aut Carboxyl‐Terminal Modulator Protein Ameliorates Pathological Cardiac Hypertrophy by Suppressing the Protein Kinase B Signaling Pathway 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Carboxyl‐terminal modulator protein (CTMP) has been implicated in cancer, brain injury, and obesity. However, the role of CTMP in pathological cardiac hypertrophy has not been identified. Methods and Results In this study, decreased expression of CTMP was observed in both human failing hearts and murine hypertrophied hearts. To further explore the potential involvement of CTMP in pathological cardiac hypertrophy, cardiac‐specific CTMP knockout and overexpression mice were generated. In vivo experiments revealed that CTMP deficiency exacerbated the cardiac hypertrophy, fibrosis, and function induced by pressure overload, whereas CTMP overexpression alleviated the response to hypertrophic stimuli. Consistent with the in vivo results, adenovirus‐mediated gain‐of‐function or loss‐of‐function experiments showed that CTMP also exerted a protective effect against hypertrophic responses to angiotensin II in vitro. Mechanistically, CTMP ameliorated pathological cardiac hypertrophy through the blockade of the protein kinase B signaling pathway. Moreover, inhibition of protein kinase B activation with LY294002 rescued the deteriorated effect in aortic banding–treated cardiac‐specific CTMP knockout mice. Conclusions Taken together, these findings imply, for the first time, that increasing the cardiac expression of CTMP may be a novel therapeutic strategy for pathological cardiac hypertrophy. angiotensin II aortic banding carboxyl‐terminal modulator protein pathological cardiac hypertrophy signal transduction Diseases of the circulatory (Cardiovascular) system Qin Yang verfasserin aut Li‐Hua Zhu verfasserin aut Jia Liu verfasserin aut Ke‐Qiong Deng verfasserin aut Xue‐Yong Zhu verfasserin aut Ye Liu verfasserin aut Jun Gong verfasserin aut Peng Zhang verfasserin aut Shuyan Li verfasserin aut Hao Xia verfasserin aut Zhi‐Gang She verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 7(2018), 13 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:7 year:2018 number:13 https://doi.org/10.1161/JAHA.118.008654 kostenfrei https://doaj.org/article/88882cacec304168b65de30be4e8ce31 kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.118.008654 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_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_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_2049 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_2336 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 7 2018 13
language	English
source	In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease 7(2018), 13 volume:7 year:2018 number:13
sourceStr	In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease 7(2018), 13 volume:7 year:2018 number:13
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	angiotensin II aortic banding carboxyl‐terminal modulator protein pathological cardiac hypertrophy signal transduction Diseases of the circulatory (Cardiovascular) system
isfreeaccess_bool	true
container_title	Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
authorswithroles_txt_mv	Xiaoxiong Liu @@aut@@ Qin Yang @@aut@@ Li‐Hua Zhu @@aut@@ Jia Liu @@aut@@ Ke‐Qiong Deng @@aut@@ Xue‐Yong Zhu @@aut@@ Ye Liu @@aut@@ Jun Gong @@aut@@ Peng Zhang @@aut@@ Shuyan Li @@aut@@ Hao Xia @@aut@@ Zhi‐Gang She @@aut@@
publishDateDaySort_date	2018-01-01T00:00:00Z
hierarchy_top_id	688605427
id	DOAJ007565224
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ007565224</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230309233552.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230225s2018 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1161/JAHA.118.008654</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ007565224</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ88882cacec304168b65de30be4e8ce31</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC666-701</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Xiaoxiong Liu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Carboxyl‐Terminal Modulator Protein Ameliorates Pathological Cardiac Hypertrophy by Suppressing the Protein Kinase B Signaling Pathway</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Carboxyl‐terminal modulator protein (CTMP) has been implicated in cancer, brain injury, and obesity. However, the role of CTMP in pathological cardiac hypertrophy has not been identified. Methods and Results In this study, decreased expression of CTMP was observed in both human failing hearts and murine hypertrophied hearts. To further explore the potential involvement of CTMP in pathological cardiac hypertrophy, cardiac‐specific CTMP knockout and overexpression mice were generated. In vivo experiments revealed that CTMP deficiency exacerbated the cardiac hypertrophy, fibrosis, and function induced by pressure overload, whereas CTMP overexpression alleviated the response to hypertrophic stimuli. Consistent with the in vivo results, adenovirus‐mediated gain‐of‐function or loss‐of‐function experiments showed that CTMP also exerted a protective effect against hypertrophic responses to angiotensin II in vitro. Mechanistically, CTMP ameliorated pathological cardiac hypertrophy through the blockade of the protein kinase B signaling pathway. Moreover, inhibition of protein kinase B activation with LY294002 rescued the deteriorated effect in aortic banding–treated cardiac‐specific CTMP knockout mice. Conclusions Taken together, these findings imply, for the first time, that increasing the cardiac expression of CTMP may be a novel therapeutic strategy for pathological cardiac hypertrophy.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">angiotensin II</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">aortic banding</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">carboxyl‐terminal modulator protein</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">pathological cardiac hypertrophy</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">signal transduction</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Diseases of the circulatory (Cardiovascular) system</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Qin Yang</subfield><subfield code="e">verfasserin</subfield><subfield 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callnumber-first	R - Medicine
author	Xiaoxiong Liu
spellingShingle	Xiaoxiong Liu misc RC666-701 misc angiotensin II misc aortic banding misc carboxyl‐terminal modulator protein misc pathological cardiac hypertrophy misc signal transduction misc Diseases of the circulatory (Cardiovascular) system Carboxyl‐Terminal Modulator Protein Ameliorates Pathological Cardiac Hypertrophy by Suppressing the Protein Kinase B Signaling Pathway
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topic_title	RC666-701 Carboxyl‐Terminal Modulator Protein Ameliorates Pathological Cardiac Hypertrophy by Suppressing the Protein Kinase B Signaling Pathway angiotensin II aortic banding carboxyl‐terminal modulator protein pathological cardiac hypertrophy signal transduction
topic	misc RC666-701 misc angiotensin II misc aortic banding misc carboxyl‐terminal modulator protein misc pathological cardiac hypertrophy misc signal transduction misc Diseases of the circulatory (Cardiovascular) system
topic_unstemmed	misc RC666-701 misc angiotensin II misc aortic banding misc carboxyl‐terminal modulator protein misc pathological cardiac hypertrophy misc signal transduction misc Diseases of the circulatory (Cardiovascular) system
topic_browse	misc RC666-701 misc angiotensin II misc aortic banding misc carboxyl‐terminal modulator protein misc pathological cardiac hypertrophy misc signal transduction misc Diseases of the circulatory (Cardiovascular) system
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title	Carboxyl‐Terminal Modulator Protein Ameliorates Pathological Cardiac Hypertrophy by Suppressing the Protein Kinase B Signaling Pathway
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title_full	Carboxyl‐Terminal Modulator Protein Ameliorates Pathological Cardiac Hypertrophy by Suppressing the Protein Kinase B Signaling Pathway
author_sort	Xiaoxiong Liu
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author_browse	Xiaoxiong Liu Qin Yang Li‐Hua Zhu Jia Liu Ke‐Qiong Deng Xue‐Yong Zhu Ye Liu Jun Gong Peng Zhang Shuyan Li Hao Xia Zhi‐Gang She
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title_sort	carboxyl‐terminal modulator protein ameliorates pathological cardiac hypertrophy by suppressing the protein kinase b signaling pathway
callnumber	RC666-701
title_auth	Carboxyl‐Terminal Modulator Protein Ameliorates Pathological Cardiac Hypertrophy by Suppressing the Protein Kinase B Signaling Pathway
abstract	Background Carboxyl‐terminal modulator protein (CTMP) has been implicated in cancer, brain injury, and obesity. However, the role of CTMP in pathological cardiac hypertrophy has not been identified. Methods and Results In this study, decreased expression of CTMP was observed in both human failing hearts and murine hypertrophied hearts. To further explore the potential involvement of CTMP in pathological cardiac hypertrophy, cardiac‐specific CTMP knockout and overexpression mice were generated. In vivo experiments revealed that CTMP deficiency exacerbated the cardiac hypertrophy, fibrosis, and function induced by pressure overload, whereas CTMP overexpression alleviated the response to hypertrophic stimuli. Consistent with the in vivo results, adenovirus‐mediated gain‐of‐function or loss‐of‐function experiments showed that CTMP also exerted a protective effect against hypertrophic responses to angiotensin II in vitro. Mechanistically, CTMP ameliorated pathological cardiac hypertrophy through the blockade of the protein kinase B signaling pathway. Moreover, inhibition of protein kinase B activation with LY294002 rescued the deteriorated effect in aortic banding–treated cardiac‐specific CTMP knockout mice. Conclusions Taken together, these findings imply, for the first time, that increasing the cardiac expression of CTMP may be a novel therapeutic strategy for pathological cardiac hypertrophy.
abstractGer	Background Carboxyl‐terminal modulator protein (CTMP) has been implicated in cancer, brain injury, and obesity. However, the role of CTMP in pathological cardiac hypertrophy has not been identified. Methods and Results In this study, decreased expression of CTMP was observed in both human failing hearts and murine hypertrophied hearts. To further explore the potential involvement of CTMP in pathological cardiac hypertrophy, cardiac‐specific CTMP knockout and overexpression mice were generated. In vivo experiments revealed that CTMP deficiency exacerbated the cardiac hypertrophy, fibrosis, and function induced by pressure overload, whereas CTMP overexpression alleviated the response to hypertrophic stimuli. Consistent with the in vivo results, adenovirus‐mediated gain‐of‐function or loss‐of‐function experiments showed that CTMP also exerted a protective effect against hypertrophic responses to angiotensin II in vitro. Mechanistically, CTMP ameliorated pathological cardiac hypertrophy through the blockade of the protein kinase B signaling pathway. Moreover, inhibition of protein kinase B activation with LY294002 rescued the deteriorated effect in aortic banding–treated cardiac‐specific CTMP knockout mice. Conclusions Taken together, these findings imply, for the first time, that increasing the cardiac expression of CTMP may be a novel therapeutic strategy for pathological cardiac hypertrophy.
abstract_unstemmed	Background Carboxyl‐terminal modulator protein (CTMP) has been implicated in cancer, brain injury, and obesity. However, the role of CTMP in pathological cardiac hypertrophy has not been identified. Methods and Results In this study, decreased expression of CTMP was observed in both human failing hearts and murine hypertrophied hearts. To further explore the potential involvement of CTMP in pathological cardiac hypertrophy, cardiac‐specific CTMP knockout and overexpression mice were generated. In vivo experiments revealed that CTMP deficiency exacerbated the cardiac hypertrophy, fibrosis, and function induced by pressure overload, whereas CTMP overexpression alleviated the response to hypertrophic stimuli. Consistent with the in vivo results, adenovirus‐mediated gain‐of‐function or loss‐of‐function experiments showed that CTMP also exerted a protective effect against hypertrophic responses to angiotensin II in vitro. Mechanistically, CTMP ameliorated pathological cardiac hypertrophy through the blockade of the protein kinase B signaling pathway. Moreover, inhibition of protein kinase B activation with LY294002 rescued the deteriorated effect in aortic banding–treated cardiac‐specific CTMP knockout mice. Conclusions Taken together, these findings imply, for the first time, that increasing the cardiac expression of CTMP may be a novel therapeutic strategy for pathological cardiac hypertrophy.
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title_short	Carboxyl‐Terminal Modulator Protein Ameliorates Pathological Cardiac Hypertrophy by Suppressing the Protein Kinase B Signaling Pathway
url	https://doi.org/10.1161/JAHA.118.008654 https://doaj.org/article/88882cacec304168b65de30be4e8ce31 https://www.ahajournals.org/doi/10.1161/JAHA.118.008654 https://doaj.org/toc/2047-9980
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up_date	2024-07-04T02:03:05.774Z
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fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ007565224</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230309233552.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230225s2018 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1161/JAHA.118.008654</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ007565224</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ88882cacec304168b65de30be4e8ce31</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC666-701</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Xiaoxiong Liu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Carboxyl‐Terminal Modulator Protein Ameliorates Pathological Cardiac Hypertrophy by Suppressing the Protein Kinase B Signaling Pathway</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Carboxyl‐terminal modulator protein (CTMP) has been implicated in cancer, brain injury, and obesity. However, the role of CTMP in pathological cardiac hypertrophy has not been identified. Methods and Results In this study, decreased expression of CTMP was observed in both human failing hearts and murine hypertrophied hearts. To further explore the potential involvement of CTMP in pathological cardiac hypertrophy, cardiac‐specific CTMP knockout and overexpression mice were generated. In vivo experiments revealed that CTMP deficiency exacerbated the cardiac hypertrophy, fibrosis, and function induced by pressure overload, whereas CTMP overexpression alleviated the response to hypertrophic stimuli. Consistent with the in vivo results, adenovirus‐mediated gain‐of‐function or loss‐of‐function experiments showed that CTMP also exerted a protective effect against hypertrophic responses to angiotensin II in vitro. Mechanistically, CTMP ameliorated pathological cardiac hypertrophy through the blockade of the protein kinase B signaling pathway. Moreover, inhibition of protein kinase B activation with LY294002 rescued the deteriorated effect in aortic banding–treated cardiac‐specific CTMP knockout mice. Conclusions Taken together, these findings imply, for the first time, that increasing the cardiac expression of CTMP may be a novel therapeutic strategy for pathological cardiac hypertrophy.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">angiotensin II</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">aortic banding</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">carboxyl‐terminal modulator protein</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">pathological cardiac hypertrophy</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">signal transduction</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Diseases of the circulatory (Cardiovascular) system</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Qin Yang</subfield><subfield code="e">verfasserin</subfield><subfield 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Carboxyl‐Terminal Modulator Protein Ameliorates Pathological Cardiac Hypertrophy by Suppressing the Protein Kinase B Signaling Pathway

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