VEGF‐C/VEGFR‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis

Abstract Prolonged pressure overload triggers cardiac hypertrophy and frequently leads to heart failure (HF). Vascular endothelial growth factor‐C (VEGF‐C) and its receptor VEGFR‐3 are components of the central pathway for lymphatic vessel growth (also known as lymphangiogenesis), which has crucial...
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Autor*in:	Qiu‐Yue Lin [verfasserIn] Yun‐Long Zhang [verfasserIn] Jie Bai [verfasserIn] Jin‐Qiu Liu [verfasserIn] Hui‐Hua Li [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	cardiac lymphangiogenesis heart failure pressure overload VEGF‐C VEGFR‐3

Übergeordnetes Werk:	In: Clinical and Translational Medicine - Wiley, 2013, 11(2021), 3, Seite n/a-n/a
Übergeordnetes Werk:	volume:11 ; year:2021 ; number:3 ; pages:n/a-n/a

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1002/ctm2.374

Katalog-ID:	DOAJ056835825

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520			\|a Abstract Prolonged pressure overload triggers cardiac hypertrophy and frequently leads to heart failure (HF). Vascular endothelial growth factor‐C (VEGF‐C) and its receptor VEGFR‐3 are components of the central pathway for lymphatic vessel growth (also known as lymphangiogenesis), which has crucial functions in the maintenance of tissue fluid balance and myocardial function after ischemic injury. However, the roles of this pathway in the development of cardiac hypertrophy and dysfunction during pressure overload remain largely unknown. Eight‐ to 10‐week‐old male wild‐type (WT) mice, VEGFR‐3 knockdown (VEGFR‐3f/−) mice, and their WT littermates (VEGFR‐3f/f) were subjected to pressure overload induced by transverse aortic constriction (TAC) for 1–6 weeks. We found that cardiac lymphangiogenesis and the protein expression of VEGF‐C and VEGFR‐3 were upregulated in the early stage of cardiac hypertrophy but were markedly reduced in failing hearts. Moreover, TAC for 6 weeks significantly reduced cardiac lymphangiogenesis by inhibiting activation of VEGFR‐3‐mediated signals (AKT/ERK1/2, calcineurin A/NFATc1/FOXc2, and CX43), leading to increased cardiac edema, hypertrophy, fibrosis, apoptosis, inflammation, and dysfunction. These effects were further aggravated in VEGFR‐3f/− mice and were dose‐dependently attenuated by delivery of recombinant VEGF‐C156S in WT mice. VEGF‐C156s administration also reversed pre‐established cardiac dysfunction induced by sustained pressure overload. Thus, these results demonstrate, for the first time, that activation of the VEGF‐C‐VEGFR‐3 axis exerts a protective effect during the transition from cardiac hypertrophy to HF and highlight selective stimulation of cardiac lymphangiogenesis as a potential new therapeutic approach for hypertrophic heart diseases.
650		4	\|a cardiac lymphangiogenesis
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allfields	10.1002/ctm2.374 doi (DE-627)DOAJ056835825 (DE-599)DOAJ187d40ac49e34977962a80a4bc46d3c0 DE-627 ger DE-627 rakwb eng R5-920 Qiu‐Yue Lin verfasserin aut VEGF‐C/VEGFR‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Prolonged pressure overload triggers cardiac hypertrophy and frequently leads to heart failure (HF). Vascular endothelial growth factor‐C (VEGF‐C) and its receptor VEGFR‐3 are components of the central pathway for lymphatic vessel growth (also known as lymphangiogenesis), which has crucial functions in the maintenance of tissue fluid balance and myocardial function after ischemic injury. However, the roles of this pathway in the development of cardiac hypertrophy and dysfunction during pressure overload remain largely unknown. Eight‐ to 10‐week‐old male wild‐type (WT) mice, VEGFR‐3 knockdown (VEGFR‐3f/−) mice, and their WT littermates (VEGFR‐3f/f) were subjected to pressure overload induced by transverse aortic constriction (TAC) for 1–6 weeks. We found that cardiac lymphangiogenesis and the protein expression of VEGF‐C and VEGFR‐3 were upregulated in the early stage of cardiac hypertrophy but were markedly reduced in failing hearts. Moreover, TAC for 6 weeks significantly reduced cardiac lymphangiogenesis by inhibiting activation of VEGFR‐3‐mediated signals (AKT/ERK1/2, calcineurin A/NFATc1/FOXc2, and CX43), leading to increased cardiac edema, hypertrophy, fibrosis, apoptosis, inflammation, and dysfunction. These effects were further aggravated in VEGFR‐3f/− mice and were dose‐dependently attenuated by delivery of recombinant VEGF‐C156S in WT mice. VEGF‐C156s administration also reversed pre‐established cardiac dysfunction induced by sustained pressure overload. Thus, these results demonstrate, for the first time, that activation of the VEGF‐C‐VEGFR‐3 axis exerts a protective effect during the transition from cardiac hypertrophy to HF and highlight selective stimulation of cardiac lymphangiogenesis as a potential new therapeutic approach for hypertrophic heart diseases. cardiac lymphangiogenesis heart failure pressure overload VEGF‐C VEGFR‐3 Medicine (General) Yun‐Long Zhang verfasserin aut Jie Bai verfasserin aut Jin‐Qiu Liu verfasserin aut Hui‐Hua Li verfasserin aut In Clinical and Translational Medicine Wiley, 2013 11(2021), 3, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:11 year:2021 number:3 pages:n/a-n/a https://doi.org/10.1002/ctm2.374 kostenfrei https://doaj.org/article/187d40ac49e34977962a80a4bc46d3c0 kostenfrei https://doi.org/10.1002/ctm2.374 kostenfrei https://doaj.org/toc/2001-1326 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_2009 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_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 11 2021 3 n/a-n/a
spelling	10.1002/ctm2.374 doi (DE-627)DOAJ056835825 (DE-599)DOAJ187d40ac49e34977962a80a4bc46d3c0 DE-627 ger DE-627 rakwb eng R5-920 Qiu‐Yue Lin verfasserin aut VEGF‐C/VEGFR‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Prolonged pressure overload triggers cardiac hypertrophy and frequently leads to heart failure (HF). Vascular endothelial growth factor‐C (VEGF‐C) and its receptor VEGFR‐3 are components of the central pathway for lymphatic vessel growth (also known as lymphangiogenesis), which has crucial functions in the maintenance of tissue fluid balance and myocardial function after ischemic injury. However, the roles of this pathway in the development of cardiac hypertrophy and dysfunction during pressure overload remain largely unknown. Eight‐ to 10‐week‐old male wild‐type (WT) mice, VEGFR‐3 knockdown (VEGFR‐3f/−) mice, and their WT littermates (VEGFR‐3f/f) were subjected to pressure overload induced by transverse aortic constriction (TAC) for 1–6 weeks. We found that cardiac lymphangiogenesis and the protein expression of VEGF‐C and VEGFR‐3 were upregulated in the early stage of cardiac hypertrophy but were markedly reduced in failing hearts. Moreover, TAC for 6 weeks significantly reduced cardiac lymphangiogenesis by inhibiting activation of VEGFR‐3‐mediated signals (AKT/ERK1/2, calcineurin A/NFATc1/FOXc2, and CX43), leading to increased cardiac edema, hypertrophy, fibrosis, apoptosis, inflammation, and dysfunction. These effects were further aggravated in VEGFR‐3f/− mice and were dose‐dependently attenuated by delivery of recombinant VEGF‐C156S in WT mice. VEGF‐C156s administration also reversed pre‐established cardiac dysfunction induced by sustained pressure overload. Thus, these results demonstrate, for the first time, that activation of the VEGF‐C‐VEGFR‐3 axis exerts a protective effect during the transition from cardiac hypertrophy to HF and highlight selective stimulation of cardiac lymphangiogenesis as a potential new therapeutic approach for hypertrophic heart diseases. cardiac lymphangiogenesis heart failure pressure overload VEGF‐C VEGFR‐3 Medicine (General) Yun‐Long Zhang verfasserin aut Jie Bai verfasserin aut Jin‐Qiu Liu verfasserin aut Hui‐Hua Li verfasserin aut In Clinical and Translational Medicine Wiley, 2013 11(2021), 3, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:11 year:2021 number:3 pages:n/a-n/a https://doi.org/10.1002/ctm2.374 kostenfrei https://doaj.org/article/187d40ac49e34977962a80a4bc46d3c0 kostenfrei https://doi.org/10.1002/ctm2.374 kostenfrei https://doaj.org/toc/2001-1326 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_2009 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_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 11 2021 3 n/a-n/a
allfields_unstemmed	10.1002/ctm2.374 doi (DE-627)DOAJ056835825 (DE-599)DOAJ187d40ac49e34977962a80a4bc46d3c0 DE-627 ger DE-627 rakwb eng R5-920 Qiu‐Yue Lin verfasserin aut VEGF‐C/VEGFR‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Prolonged pressure overload triggers cardiac hypertrophy and frequently leads to heart failure (HF). Vascular endothelial growth factor‐C (VEGF‐C) and its receptor VEGFR‐3 are components of the central pathway for lymphatic vessel growth (also known as lymphangiogenesis), which has crucial functions in the maintenance of tissue fluid balance and myocardial function after ischemic injury. However, the roles of this pathway in the development of cardiac hypertrophy and dysfunction during pressure overload remain largely unknown. Eight‐ to 10‐week‐old male wild‐type (WT) mice, VEGFR‐3 knockdown (VEGFR‐3f/−) mice, and their WT littermates (VEGFR‐3f/f) were subjected to pressure overload induced by transverse aortic constriction (TAC) for 1–6 weeks. We found that cardiac lymphangiogenesis and the protein expression of VEGF‐C and VEGFR‐3 were upregulated in the early stage of cardiac hypertrophy but were markedly reduced in failing hearts. Moreover, TAC for 6 weeks significantly reduced cardiac lymphangiogenesis by inhibiting activation of VEGFR‐3‐mediated signals (AKT/ERK1/2, calcineurin A/NFATc1/FOXc2, and CX43), leading to increased cardiac edema, hypertrophy, fibrosis, apoptosis, inflammation, and dysfunction. These effects were further aggravated in VEGFR‐3f/− mice and were dose‐dependently attenuated by delivery of recombinant VEGF‐C156S in WT mice. VEGF‐C156s administration also reversed pre‐established cardiac dysfunction induced by sustained pressure overload. Thus, these results demonstrate, for the first time, that activation of the VEGF‐C‐VEGFR‐3 axis exerts a protective effect during the transition from cardiac hypertrophy to HF and highlight selective stimulation of cardiac lymphangiogenesis as a potential new therapeutic approach for hypertrophic heart diseases. cardiac lymphangiogenesis heart failure pressure overload VEGF‐C VEGFR‐3 Medicine (General) Yun‐Long Zhang verfasserin aut Jie Bai verfasserin aut Jin‐Qiu Liu verfasserin aut Hui‐Hua Li verfasserin aut In Clinical and Translational Medicine Wiley, 2013 11(2021), 3, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:11 year:2021 number:3 pages:n/a-n/a https://doi.org/10.1002/ctm2.374 kostenfrei https://doaj.org/article/187d40ac49e34977962a80a4bc46d3c0 kostenfrei https://doi.org/10.1002/ctm2.374 kostenfrei https://doaj.org/toc/2001-1326 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_2009 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_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 11 2021 3 n/a-n/a
allfieldsGer	10.1002/ctm2.374 doi (DE-627)DOAJ056835825 (DE-599)DOAJ187d40ac49e34977962a80a4bc46d3c0 DE-627 ger DE-627 rakwb eng R5-920 Qiu‐Yue Lin verfasserin aut VEGF‐C/VEGFR‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Prolonged pressure overload triggers cardiac hypertrophy and frequently leads to heart failure (HF). Vascular endothelial growth factor‐C (VEGF‐C) and its receptor VEGFR‐3 are components of the central pathway for lymphatic vessel growth (also known as lymphangiogenesis), which has crucial functions in the maintenance of tissue fluid balance and myocardial function after ischemic injury. However, the roles of this pathway in the development of cardiac hypertrophy and dysfunction during pressure overload remain largely unknown. Eight‐ to 10‐week‐old male wild‐type (WT) mice, VEGFR‐3 knockdown (VEGFR‐3f/−) mice, and their WT littermates (VEGFR‐3f/f) were subjected to pressure overload induced by transverse aortic constriction (TAC) for 1–6 weeks. We found that cardiac lymphangiogenesis and the protein expression of VEGF‐C and VEGFR‐3 were upregulated in the early stage of cardiac hypertrophy but were markedly reduced in failing hearts. Moreover, TAC for 6 weeks significantly reduced cardiac lymphangiogenesis by inhibiting activation of VEGFR‐3‐mediated signals (AKT/ERK1/2, calcineurin A/NFATc1/FOXc2, and CX43), leading to increased cardiac edema, hypertrophy, fibrosis, apoptosis, inflammation, and dysfunction. These effects were further aggravated in VEGFR‐3f/− mice and were dose‐dependently attenuated by delivery of recombinant VEGF‐C156S in WT mice. VEGF‐C156s administration also reversed pre‐established cardiac dysfunction induced by sustained pressure overload. Thus, these results demonstrate, for the first time, that activation of the VEGF‐C‐VEGFR‐3 axis exerts a protective effect during the transition from cardiac hypertrophy to HF and highlight selective stimulation of cardiac lymphangiogenesis as a potential new therapeutic approach for hypertrophic heart diseases. cardiac lymphangiogenesis heart failure pressure overload VEGF‐C VEGFR‐3 Medicine (General) Yun‐Long Zhang verfasserin aut Jie Bai verfasserin aut Jin‐Qiu Liu verfasserin aut Hui‐Hua Li verfasserin aut In Clinical and Translational Medicine Wiley, 2013 11(2021), 3, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:11 year:2021 number:3 pages:n/a-n/a https://doi.org/10.1002/ctm2.374 kostenfrei https://doaj.org/article/187d40ac49e34977962a80a4bc46d3c0 kostenfrei https://doi.org/10.1002/ctm2.374 kostenfrei https://doaj.org/toc/2001-1326 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_2009 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_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 11 2021 3 n/a-n/a
allfieldsSound	10.1002/ctm2.374 doi (DE-627)DOAJ056835825 (DE-599)DOAJ187d40ac49e34977962a80a4bc46d3c0 DE-627 ger DE-627 rakwb eng R5-920 Qiu‐Yue Lin verfasserin aut VEGF‐C/VEGFR‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Prolonged pressure overload triggers cardiac hypertrophy and frequently leads to heart failure (HF). Vascular endothelial growth factor‐C (VEGF‐C) and its receptor VEGFR‐3 are components of the central pathway for lymphatic vessel growth (also known as lymphangiogenesis), which has crucial functions in the maintenance of tissue fluid balance and myocardial function after ischemic injury. However, the roles of this pathway in the development of cardiac hypertrophy and dysfunction during pressure overload remain largely unknown. Eight‐ to 10‐week‐old male wild‐type (WT) mice, VEGFR‐3 knockdown (VEGFR‐3f/−) mice, and their WT littermates (VEGFR‐3f/f) were subjected to pressure overload induced by transverse aortic constriction (TAC) for 1–6 weeks. We found that cardiac lymphangiogenesis and the protein expression of VEGF‐C and VEGFR‐3 were upregulated in the early stage of cardiac hypertrophy but were markedly reduced in failing hearts. Moreover, TAC for 6 weeks significantly reduced cardiac lymphangiogenesis by inhibiting activation of VEGFR‐3‐mediated signals (AKT/ERK1/2, calcineurin A/NFATc1/FOXc2, and CX43), leading to increased cardiac edema, hypertrophy, fibrosis, apoptosis, inflammation, and dysfunction. These effects were further aggravated in VEGFR‐3f/− mice and were dose‐dependently attenuated by delivery of recombinant VEGF‐C156S in WT mice. VEGF‐C156s administration also reversed pre‐established cardiac dysfunction induced by sustained pressure overload. Thus, these results demonstrate, for the first time, that activation of the VEGF‐C‐VEGFR‐3 axis exerts a protective effect during the transition from cardiac hypertrophy to HF and highlight selective stimulation of cardiac lymphangiogenesis as a potential new therapeutic approach for hypertrophic heart diseases. cardiac lymphangiogenesis heart failure pressure overload VEGF‐C VEGFR‐3 Medicine (General) Yun‐Long Zhang verfasserin aut Jie Bai verfasserin aut Jin‐Qiu Liu verfasserin aut Hui‐Hua Li verfasserin aut In Clinical and Translational Medicine Wiley, 2013 11(2021), 3, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:11 year:2021 number:3 pages:n/a-n/a https://doi.org/10.1002/ctm2.374 kostenfrei https://doaj.org/article/187d40ac49e34977962a80a4bc46d3c0 kostenfrei https://doi.org/10.1002/ctm2.374 kostenfrei https://doaj.org/toc/2001-1326 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_2009 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_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 11 2021 3 n/a-n/a
language	English
source	In Clinical and Translational Medicine 11(2021), 3, Seite n/a-n/a volume:11 year:2021 number:3 pages:n/a-n/a
sourceStr	In Clinical and Translational Medicine 11(2021), 3, Seite n/a-n/a volume:11 year:2021 number:3 pages:n/a-n/a
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	cardiac lymphangiogenesis heart failure pressure overload VEGF‐C VEGFR‐3 Medicine (General)
isfreeaccess_bool	true
container_title	Clinical and Translational Medicine
authorswithroles_txt_mv	Qiu‐Yue Lin @@aut@@ Yun‐Long Zhang @@aut@@ Jie Bai @@aut@@ Jin‐Qiu Liu @@aut@@ Hui‐Hua Li @@aut@@
publishDateDaySort_date	2021-01-01T00:00:00Z
hierarchy_top_id	733752837
id	DOAJ056835825
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">DOAJ056835825</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230308204323.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2021 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1002/ctm2.374</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ056835825</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ187d40ac49e34977962a80a4bc46d3c0</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">R5-920</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Qiu‐Yue Lin</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">VEGF‐C/VEGFR‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2021</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">Abstract Prolonged pressure overload triggers cardiac hypertrophy and frequently leads to heart failure (HF). Vascular endothelial growth factor‐C (VEGF‐C) and its receptor VEGFR‐3 are components of the central pathway for lymphatic vessel growth (also known as lymphangiogenesis), which has crucial functions in the maintenance of tissue fluid balance and myocardial function after ischemic injury. However, the roles of this pathway in the development of cardiac hypertrophy and dysfunction during pressure overload remain largely unknown. Eight‐ to 10‐week‐old male wild‐type (WT) mice, VEGFR‐3 knockdown (VEGFR‐3f/−) mice, and their WT littermates (VEGFR‐3f/f) were subjected to pressure overload induced by transverse aortic constriction (TAC) for 1–6 weeks. We found that cardiac lymphangiogenesis and the protein expression of VEGF‐C and VEGFR‐3 were upregulated in the early stage of cardiac hypertrophy but were markedly reduced in failing hearts. Moreover, TAC for 6 weeks significantly reduced cardiac lymphangiogenesis by inhibiting activation of VEGFR‐3‐mediated signals (AKT/ERK1/2, calcineurin A/NFATc1/FOXc2, and CX43), leading to increased cardiac edema, hypertrophy, fibrosis, apoptosis, inflammation, and dysfunction. These effects were further aggravated in VEGFR‐3f/− mice and were dose‐dependently attenuated by delivery of recombinant VEGF‐C156S in WT mice. VEGF‐C156s administration also reversed pre‐established cardiac dysfunction induced by sustained pressure overload. 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callnumber-first	R - Medicine
author	Qiu‐Yue Lin
spellingShingle	Qiu‐Yue Lin misc R5-920 misc cardiac lymphangiogenesis misc heart failure misc pressure overload misc VEGF‐C misc VEGFR‐3 misc Medicine (General) VEGF‐C/VEGFR‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis
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topic_title	R5-920 VEGF‐C/VEGFR‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis cardiac lymphangiogenesis heart failure pressure overload VEGF‐C VEGFR‐3
topic	misc R5-920 misc cardiac lymphangiogenesis misc heart failure misc pressure overload misc VEGF‐C misc VEGFR‐3 misc Medicine (General)
topic_unstemmed	misc R5-920 misc cardiac lymphangiogenesis misc heart failure misc pressure overload misc VEGF‐C misc VEGFR‐3 misc Medicine (General)
topic_browse	misc R5-920 misc cardiac lymphangiogenesis misc heart failure misc pressure overload misc VEGF‐C misc VEGFR‐3 misc Medicine (General)
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title	VEGF‐C/VEGFR‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis
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title_full	VEGF‐C/VEGFR‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis
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author_browse	Qiu‐Yue Lin Yun‐Long Zhang Jie Bai Jin‐Qiu Liu Hui‐Hua Li
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title_sort	vegf‐c/vegfr‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis
callnumber	R5-920
title_auth	VEGF‐C/VEGFR‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis
abstract	Abstract Prolonged pressure overload triggers cardiac hypertrophy and frequently leads to heart failure (HF). Vascular endothelial growth factor‐C (VEGF‐C) and its receptor VEGFR‐3 are components of the central pathway for lymphatic vessel growth (also known as lymphangiogenesis), which has crucial functions in the maintenance of tissue fluid balance and myocardial function after ischemic injury. However, the roles of this pathway in the development of cardiac hypertrophy and dysfunction during pressure overload remain largely unknown. Eight‐ to 10‐week‐old male wild‐type (WT) mice, VEGFR‐3 knockdown (VEGFR‐3f/−) mice, and their WT littermates (VEGFR‐3f/f) were subjected to pressure overload induced by transverse aortic constriction (TAC) for 1–6 weeks. We found that cardiac lymphangiogenesis and the protein expression of VEGF‐C and VEGFR‐3 were upregulated in the early stage of cardiac hypertrophy but were markedly reduced in failing hearts. Moreover, TAC for 6 weeks significantly reduced cardiac lymphangiogenesis by inhibiting activation of VEGFR‐3‐mediated signals (AKT/ERK1/2, calcineurin A/NFATc1/FOXc2, and CX43), leading to increased cardiac edema, hypertrophy, fibrosis, apoptosis, inflammation, and dysfunction. These effects were further aggravated in VEGFR‐3f/− mice and were dose‐dependently attenuated by delivery of recombinant VEGF‐C156S in WT mice. VEGF‐C156s administration also reversed pre‐established cardiac dysfunction induced by sustained pressure overload. Thus, these results demonstrate, for the first time, that activation of the VEGF‐C‐VEGFR‐3 axis exerts a protective effect during the transition from cardiac hypertrophy to HF and highlight selective stimulation of cardiac lymphangiogenesis as a potential new therapeutic approach for hypertrophic heart diseases.
abstractGer	Abstract Prolonged pressure overload triggers cardiac hypertrophy and frequently leads to heart failure (HF). Vascular endothelial growth factor‐C (VEGF‐C) and its receptor VEGFR‐3 are components of the central pathway for lymphatic vessel growth (also known as lymphangiogenesis), which has crucial functions in the maintenance of tissue fluid balance and myocardial function after ischemic injury. However, the roles of this pathway in the development of cardiac hypertrophy and dysfunction during pressure overload remain largely unknown. Eight‐ to 10‐week‐old male wild‐type (WT) mice, VEGFR‐3 knockdown (VEGFR‐3f/−) mice, and their WT littermates (VEGFR‐3f/f) were subjected to pressure overload induced by transverse aortic constriction (TAC) for 1–6 weeks. We found that cardiac lymphangiogenesis and the protein expression of VEGF‐C and VEGFR‐3 were upregulated in the early stage of cardiac hypertrophy but were markedly reduced in failing hearts. Moreover, TAC for 6 weeks significantly reduced cardiac lymphangiogenesis by inhibiting activation of VEGFR‐3‐mediated signals (AKT/ERK1/2, calcineurin A/NFATc1/FOXc2, and CX43), leading to increased cardiac edema, hypertrophy, fibrosis, apoptosis, inflammation, and dysfunction. These effects were further aggravated in VEGFR‐3f/− mice and were dose‐dependently attenuated by delivery of recombinant VEGF‐C156S in WT mice. VEGF‐C156s administration also reversed pre‐established cardiac dysfunction induced by sustained pressure overload. Thus, these results demonstrate, for the first time, that activation of the VEGF‐C‐VEGFR‐3 axis exerts a protective effect during the transition from cardiac hypertrophy to HF and highlight selective stimulation of cardiac lymphangiogenesis as a potential new therapeutic approach for hypertrophic heart diseases.
abstract_unstemmed	Abstract Prolonged pressure overload triggers cardiac hypertrophy and frequently leads to heart failure (HF). Vascular endothelial growth factor‐C (VEGF‐C) and its receptor VEGFR‐3 are components of the central pathway for lymphatic vessel growth (also known as lymphangiogenesis), which has crucial functions in the maintenance of tissue fluid balance and myocardial function after ischemic injury. However, the roles of this pathway in the development of cardiac hypertrophy and dysfunction during pressure overload remain largely unknown. Eight‐ to 10‐week‐old male wild‐type (WT) mice, VEGFR‐3 knockdown (VEGFR‐3f/−) mice, and their WT littermates (VEGFR‐3f/f) were subjected to pressure overload induced by transverse aortic constriction (TAC) for 1–6 weeks. We found that cardiac lymphangiogenesis and the protein expression of VEGF‐C and VEGFR‐3 were upregulated in the early stage of cardiac hypertrophy but were markedly reduced in failing hearts. Moreover, TAC for 6 weeks significantly reduced cardiac lymphangiogenesis by inhibiting activation of VEGFR‐3‐mediated signals (AKT/ERK1/2, calcineurin A/NFATc1/FOXc2, and CX43), leading to increased cardiac edema, hypertrophy, fibrosis, apoptosis, inflammation, and dysfunction. These effects were further aggravated in VEGFR‐3f/− mice and were dose‐dependently attenuated by delivery of recombinant VEGF‐C156S in WT mice. VEGF‐C156s administration also reversed pre‐established cardiac dysfunction induced by sustained pressure overload. Thus, these results demonstrate, for the first time, that activation of the VEGF‐C‐VEGFR‐3 axis exerts a protective effect during the transition from cardiac hypertrophy to HF and highlight selective stimulation of cardiac lymphangiogenesis as a potential new therapeutic approach for hypertrophic heart diseases.
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title_short	VEGF‐C/VEGFR‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis
url	https://doi.org/10.1002/ctm2.374 https://doaj.org/article/187d40ac49e34977962a80a4bc46d3c0 https://doaj.org/toc/2001-1326
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up_date	2024-07-03T23:06:39.549Z
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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">DOAJ056835825</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230308204323.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2021 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1002/ctm2.374</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ056835825</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ187d40ac49e34977962a80a4bc46d3c0</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">R5-920</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Qiu‐Yue Lin</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">VEGF‐C/VEGFR‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2021</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">Abstract Prolonged pressure overload triggers cardiac hypertrophy and frequently leads to heart failure (HF). Vascular endothelial growth factor‐C (VEGF‐C) and its receptor VEGFR‐3 are components of the central pathway for lymphatic vessel growth (also known as lymphangiogenesis), which has crucial functions in the maintenance of tissue fluid balance and myocardial function after ischemic injury. However, the roles of this pathway in the development of cardiac hypertrophy and dysfunction during pressure overload remain largely unknown. Eight‐ to 10‐week‐old male wild‐type (WT) mice, VEGFR‐3 knockdown (VEGFR‐3f/−) mice, and their WT littermates (VEGFR‐3f/f) were subjected to pressure overload induced by transverse aortic constriction (TAC) for 1–6 weeks. We found that cardiac lymphangiogenesis and the protein expression of VEGF‐C and VEGFR‐3 were upregulated in the early stage of cardiac hypertrophy but were markedly reduced in failing hearts. Moreover, TAC for 6 weeks significantly reduced cardiac lymphangiogenesis by inhibiting activation of VEGFR‐3‐mediated signals (AKT/ERK1/2, calcineurin A/NFATc1/FOXc2, and CX43), leading to increased cardiac edema, hypertrophy, fibrosis, apoptosis, inflammation, and dysfunction. These effects were further aggravated in VEGFR‐3f/− mice and were dose‐dependently attenuated by delivery of recombinant VEGF‐C156S in WT mice. VEGF‐C156s administration also reversed pre‐established cardiac dysfunction induced by sustained pressure overload. Thus, these results demonstrate, for the first time, that activation of the VEGF‐C‐VEGFR‐3 axis exerts a protective effect during the transition from cardiac hypertrophy to HF and highlight selective stimulation of cardiac lymphangiogenesis as a potential new therapeutic approach for hypertrophic heart diseases.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">cardiac lymphangiogenesis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">heart failure</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">pressure overload</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">VEGF‐C</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">VEGFR‐3</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Medicine (General)</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Yun‐Long Zhang</subfield><subfield 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VEGF‐C/VEGFR‐3 axis protects against pressure‐overload induced cardiac dysfunction through regulation of lymphangiogenesis

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