Reactive Oxygen Species Cause Exercise-Induced Angina in a Myocardial Ischaemia-Reperfusion Injury Model

Percutaneous coronary intervention (PCI) effectively treats obstructive coronary artery syndrome. However, 30–40% patients continue to have angina after a successful PCI, thereby reducing patient satisfaction. The mechanisms underlying persistent angina after revascularisation therapy are still poor...
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Autor*in:	Xiaohang Wang [verfasserIn] Hirosato Kanda [verfasserIn] Takeshi Tsujino [verfasserIn] Yoko Kogure [verfasserIn] Feng Zhu [verfasserIn] Satoshi Yamamoto [verfasserIn] Taichi Sakaguchi [verfasserIn] Koichi Noguchi [verfasserIn] Yi Dai [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	angina post PCI exercise-induced cardiac pain p-ERK hydrogen peroxide TRPA1 myocardial I/R injury

Übergeordnetes Werk:	In: International Journal of Molecular Sciences - MDPI AG, 2003, 23(2022), 5, p 2820
Übergeordnetes Werk:	volume:23 ; year:2022 ; number:5, p 2820

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

DOI / URN:	10.3390/ijms23052820

Katalog-ID:	DOAJ016558006

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520			\|a Percutaneous coronary intervention (PCI) effectively treats obstructive coronary artery syndrome. However, 30–40% patients continue to have angina after a successful PCI, thereby reducing patient satisfaction. The mechanisms underlying persistent angina after revascularisation therapy are still poorly understood; hence, the treatment or guideline for post-PCI angina remains unestablished. Thus, this study aimed to investigate the mechanisms underlying effort angina in animals following myocardial ischaemia-reperfusion (I/R) injury. Phosphorylated extracellular signal-regulated kinase (p-ERK), a marker for painful stimulation-induced neuronal activation, was used for the investigation. After a forced treadmill exercise (FTE), the number of p-ERK-expressing neurons increased in the superficial dorsal horn of the I/R model animals. Moreover, FTE evoked hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) production in the I/R-injured heart, inducing angina through TRPA1 activation on cardiac sensory fibres. Notably, the treatment of a TEMPOL, a reactive oxygen species scavenger, or TRPA1<sup<−/−</sup< mice successfully alleviated the FTE-induced p-ERK expression in the dorsal horn. The production of H<sub<2</sub<O<sub<2</sub<, a reactive oxygen species, through physical exercise contributes to angina development following I/R. Hence, our findings may be useful for understanding and treating angina following revascularisation therapy.
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allfields	10.3390/ijms23052820 doi (DE-627)DOAJ016558006 (DE-599)DOAJd6507877de4d49539274d9c7a150121e DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Xiaohang Wang verfasserin aut Reactive Oxygen Species Cause Exercise-Induced Angina in a Myocardial Ischaemia-Reperfusion Injury Model 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Percutaneous coronary intervention (PCI) effectively treats obstructive coronary artery syndrome. However, 30–40% patients continue to have angina after a successful PCI, thereby reducing patient satisfaction. The mechanisms underlying persistent angina after revascularisation therapy are still poorly understood; hence, the treatment or guideline for post-PCI angina remains unestablished. Thus, this study aimed to investigate the mechanisms underlying effort angina in animals following myocardial ischaemia-reperfusion (I/R) injury. Phosphorylated extracellular signal-regulated kinase (p-ERK), a marker for painful stimulation-induced neuronal activation, was used for the investigation. After a forced treadmill exercise (FTE), the number of p-ERK-expressing neurons increased in the superficial dorsal horn of the I/R model animals. Moreover, FTE evoked hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) production in the I/R-injured heart, inducing angina through TRPA1 activation on cardiac sensory fibres. Notably, the treatment of a TEMPOL, a reactive oxygen species scavenger, or TRPA1<sup<−/−</sup< mice successfully alleviated the FTE-induced p-ERK expression in the dorsal horn. The production of H<sub<2</sub<O<sub<2</sub<, a reactive oxygen species, through physical exercise contributes to angina development following I/R. Hence, our findings may be useful for understanding and treating angina following revascularisation therapy. angina post PCI exercise-induced cardiac pain p-ERK hydrogen peroxide TRPA1 myocardial I/R injury Biology (General) Chemistry Hirosato Kanda verfasserin aut Takeshi Tsujino verfasserin aut Yoko Kogure verfasserin aut Feng Zhu verfasserin aut Satoshi Yamamoto verfasserin aut Taichi Sakaguchi verfasserin aut Koichi Noguchi verfasserin aut Yi Dai verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 23(2022), 5, p 2820 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:23 year:2022 number:5, p 2820 https://doi.org/10.3390/ijms23052820 kostenfrei https://doaj.org/article/d6507877de4d49539274d9c7a150121e kostenfrei https://www.mdpi.com/1422-0067/23/5/2820 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 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_70 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_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 23 2022 5, p 2820
spelling	10.3390/ijms23052820 doi (DE-627)DOAJ016558006 (DE-599)DOAJd6507877de4d49539274d9c7a150121e DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Xiaohang Wang verfasserin aut Reactive Oxygen Species Cause Exercise-Induced Angina in a Myocardial Ischaemia-Reperfusion Injury Model 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Percutaneous coronary intervention (PCI) effectively treats obstructive coronary artery syndrome. However, 30–40% patients continue to have angina after a successful PCI, thereby reducing patient satisfaction. The mechanisms underlying persistent angina after revascularisation therapy are still poorly understood; hence, the treatment or guideline for post-PCI angina remains unestablished. Thus, this study aimed to investigate the mechanisms underlying effort angina in animals following myocardial ischaemia-reperfusion (I/R) injury. Phosphorylated extracellular signal-regulated kinase (p-ERK), a marker for painful stimulation-induced neuronal activation, was used for the investigation. After a forced treadmill exercise (FTE), the number of p-ERK-expressing neurons increased in the superficial dorsal horn of the I/R model animals. Moreover, FTE evoked hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) production in the I/R-injured heart, inducing angina through TRPA1 activation on cardiac sensory fibres. Notably, the treatment of a TEMPOL, a reactive oxygen species scavenger, or TRPA1<sup<−/−</sup< mice successfully alleviated the FTE-induced p-ERK expression in the dorsal horn. The production of H<sub<2</sub<O<sub<2</sub<, a reactive oxygen species, through physical exercise contributes to angina development following I/R. Hence, our findings may be useful for understanding and treating angina following revascularisation therapy. angina post PCI exercise-induced cardiac pain p-ERK hydrogen peroxide TRPA1 myocardial I/R injury Biology (General) Chemistry Hirosato Kanda verfasserin aut Takeshi Tsujino verfasserin aut Yoko Kogure verfasserin aut Feng Zhu verfasserin aut Satoshi Yamamoto verfasserin aut Taichi Sakaguchi verfasserin aut Koichi Noguchi verfasserin aut Yi Dai verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 23(2022), 5, p 2820 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:23 year:2022 number:5, p 2820 https://doi.org/10.3390/ijms23052820 kostenfrei https://doaj.org/article/d6507877de4d49539274d9c7a150121e kostenfrei https://www.mdpi.com/1422-0067/23/5/2820 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 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_70 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_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 23 2022 5, p 2820
allfields_unstemmed	10.3390/ijms23052820 doi (DE-627)DOAJ016558006 (DE-599)DOAJd6507877de4d49539274d9c7a150121e DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Xiaohang Wang verfasserin aut Reactive Oxygen Species Cause Exercise-Induced Angina in a Myocardial Ischaemia-Reperfusion Injury Model 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Percutaneous coronary intervention (PCI) effectively treats obstructive coronary artery syndrome. However, 30–40% patients continue to have angina after a successful PCI, thereby reducing patient satisfaction. The mechanisms underlying persistent angina after revascularisation therapy are still poorly understood; hence, the treatment or guideline for post-PCI angina remains unestablished. Thus, this study aimed to investigate the mechanisms underlying effort angina in animals following myocardial ischaemia-reperfusion (I/R) injury. Phosphorylated extracellular signal-regulated kinase (p-ERK), a marker for painful stimulation-induced neuronal activation, was used for the investigation. After a forced treadmill exercise (FTE), the number of p-ERK-expressing neurons increased in the superficial dorsal horn of the I/R model animals. Moreover, FTE evoked hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) production in the I/R-injured heart, inducing angina through TRPA1 activation on cardiac sensory fibres. Notably, the treatment of a TEMPOL, a reactive oxygen species scavenger, or TRPA1<sup<−/−</sup< mice successfully alleviated the FTE-induced p-ERK expression in the dorsal horn. The production of H<sub<2</sub<O<sub<2</sub<, a reactive oxygen species, through physical exercise contributes to angina development following I/R. Hence, our findings may be useful for understanding and treating angina following revascularisation therapy. angina post PCI exercise-induced cardiac pain p-ERK hydrogen peroxide TRPA1 myocardial I/R injury Biology (General) Chemistry Hirosato Kanda verfasserin aut Takeshi Tsujino verfasserin aut Yoko Kogure verfasserin aut Feng Zhu verfasserin aut Satoshi Yamamoto verfasserin aut Taichi Sakaguchi verfasserin aut Koichi Noguchi verfasserin aut Yi Dai verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 23(2022), 5, p 2820 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:23 year:2022 number:5, p 2820 https://doi.org/10.3390/ijms23052820 kostenfrei https://doaj.org/article/d6507877de4d49539274d9c7a150121e kostenfrei https://www.mdpi.com/1422-0067/23/5/2820 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 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_70 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_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 23 2022 5, p 2820
allfieldsGer	10.3390/ijms23052820 doi (DE-627)DOAJ016558006 (DE-599)DOAJd6507877de4d49539274d9c7a150121e DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Xiaohang Wang verfasserin aut Reactive Oxygen Species Cause Exercise-Induced Angina in a Myocardial Ischaemia-Reperfusion Injury Model 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Percutaneous coronary intervention (PCI) effectively treats obstructive coronary artery syndrome. However, 30–40% patients continue to have angina after a successful PCI, thereby reducing patient satisfaction. The mechanisms underlying persistent angina after revascularisation therapy are still poorly understood; hence, the treatment or guideline for post-PCI angina remains unestablished. Thus, this study aimed to investigate the mechanisms underlying effort angina in animals following myocardial ischaemia-reperfusion (I/R) injury. Phosphorylated extracellular signal-regulated kinase (p-ERK), a marker for painful stimulation-induced neuronal activation, was used for the investigation. After a forced treadmill exercise (FTE), the number of p-ERK-expressing neurons increased in the superficial dorsal horn of the I/R model animals. Moreover, FTE evoked hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) production in the I/R-injured heart, inducing angina through TRPA1 activation on cardiac sensory fibres. Notably, the treatment of a TEMPOL, a reactive oxygen species scavenger, or TRPA1<sup<−/−</sup< mice successfully alleviated the FTE-induced p-ERK expression in the dorsal horn. The production of H<sub<2</sub<O<sub<2</sub<, a reactive oxygen species, through physical exercise contributes to angina development following I/R. Hence, our findings may be useful for understanding and treating angina following revascularisation therapy. angina post PCI exercise-induced cardiac pain p-ERK hydrogen peroxide TRPA1 myocardial I/R injury Biology (General) Chemistry Hirosato Kanda verfasserin aut Takeshi Tsujino verfasserin aut Yoko Kogure verfasserin aut Feng Zhu verfasserin aut Satoshi Yamamoto verfasserin aut Taichi Sakaguchi verfasserin aut Koichi Noguchi verfasserin aut Yi Dai verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 23(2022), 5, p 2820 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:23 year:2022 number:5, p 2820 https://doi.org/10.3390/ijms23052820 kostenfrei https://doaj.org/article/d6507877de4d49539274d9c7a150121e kostenfrei https://www.mdpi.com/1422-0067/23/5/2820 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 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_70 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_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 23 2022 5, p 2820
allfieldsSound	10.3390/ijms23052820 doi (DE-627)DOAJ016558006 (DE-599)DOAJd6507877de4d49539274d9c7a150121e DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Xiaohang Wang verfasserin aut Reactive Oxygen Species Cause Exercise-Induced Angina in a Myocardial Ischaemia-Reperfusion Injury Model 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Percutaneous coronary intervention (PCI) effectively treats obstructive coronary artery syndrome. However, 30–40% patients continue to have angina after a successful PCI, thereby reducing patient satisfaction. The mechanisms underlying persistent angina after revascularisation therapy are still poorly understood; hence, the treatment or guideline for post-PCI angina remains unestablished. Thus, this study aimed to investigate the mechanisms underlying effort angina in animals following myocardial ischaemia-reperfusion (I/R) injury. Phosphorylated extracellular signal-regulated kinase (p-ERK), a marker for painful stimulation-induced neuronal activation, was used for the investigation. After a forced treadmill exercise (FTE), the number of p-ERK-expressing neurons increased in the superficial dorsal horn of the I/R model animals. Moreover, FTE evoked hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) production in the I/R-injured heart, inducing angina through TRPA1 activation on cardiac sensory fibres. Notably, the treatment of a TEMPOL, a reactive oxygen species scavenger, or TRPA1<sup<−/−</sup< mice successfully alleviated the FTE-induced p-ERK expression in the dorsal horn. The production of H<sub<2</sub<O<sub<2</sub<, a reactive oxygen species, through physical exercise contributes to angina development following I/R. Hence, our findings may be useful for understanding and treating angina following revascularisation therapy. angina post PCI exercise-induced cardiac pain p-ERK hydrogen peroxide TRPA1 myocardial I/R injury Biology (General) Chemistry Hirosato Kanda verfasserin aut Takeshi Tsujino verfasserin aut Yoko Kogure verfasserin aut Feng Zhu verfasserin aut Satoshi Yamamoto verfasserin aut Taichi Sakaguchi verfasserin aut Koichi Noguchi verfasserin aut Yi Dai verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 23(2022), 5, p 2820 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:23 year:2022 number:5, p 2820 https://doi.org/10.3390/ijms23052820 kostenfrei https://doaj.org/article/d6507877de4d49539274d9c7a150121e kostenfrei https://www.mdpi.com/1422-0067/23/5/2820 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 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_70 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_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 23 2022 5, p 2820
language	English
source	In International Journal of Molecular Sciences 23(2022), 5, p 2820 volume:23 year:2022 number:5, p 2820
sourceStr	In International Journal of Molecular Sciences 23(2022), 5, p 2820 volume:23 year:2022 number:5, p 2820
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	angina post PCI exercise-induced cardiac pain p-ERK hydrogen peroxide TRPA1 myocardial I/R injury Biology (General) Chemistry
isfreeaccess_bool	true
container_title	International Journal of Molecular Sciences
authorswithroles_txt_mv	Xiaohang Wang @@aut@@ Hirosato Kanda @@aut@@ Takeshi Tsujino @@aut@@ Yoko Kogure @@aut@@ Feng Zhu @@aut@@ Satoshi Yamamoto @@aut@@ Taichi Sakaguchi @@aut@@ Koichi Noguchi @@aut@@ Yi Dai @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	316340715
id	DOAJ016558006
language_de	englisch
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callnumber-first	Q - Science
author	Xiaohang Wang
spellingShingle	Xiaohang Wang misc QH301-705.5 misc QD1-999 misc angina post PCI misc exercise-induced cardiac pain misc p-ERK misc hydrogen peroxide misc TRPA1 misc myocardial I/R injury misc Biology (General) misc Chemistry Reactive Oxygen Species Cause Exercise-Induced Angina in a Myocardial Ischaemia-Reperfusion Injury Model
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topic_title	QH301-705.5 QD1-999 Reactive Oxygen Species Cause Exercise-Induced Angina in a Myocardial Ischaemia-Reperfusion Injury Model angina post PCI exercise-induced cardiac pain p-ERK hydrogen peroxide TRPA1 myocardial I/R injury
topic	misc QH301-705.5 misc QD1-999 misc angina post PCI misc exercise-induced cardiac pain misc p-ERK misc hydrogen peroxide misc TRPA1 misc myocardial I/R injury misc Biology (General) misc Chemistry
topic_unstemmed	misc QH301-705.5 misc QD1-999 misc angina post PCI misc exercise-induced cardiac pain misc p-ERK misc hydrogen peroxide misc TRPA1 misc myocardial I/R injury misc Biology (General) misc Chemistry
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title	Reactive Oxygen Species Cause Exercise-Induced Angina in a Myocardial Ischaemia-Reperfusion Injury Model
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title_full	Reactive Oxygen Species Cause Exercise-Induced Angina in a Myocardial Ischaemia-Reperfusion Injury Model
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author_browse	Xiaohang Wang Hirosato Kanda Takeshi Tsujino Yoko Kogure Feng Zhu Satoshi Yamamoto Taichi Sakaguchi Koichi Noguchi Yi Dai
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title_sort	reactive oxygen species cause exercise-induced angina in a myocardial ischaemia-reperfusion injury model
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title_auth	Reactive Oxygen Species Cause Exercise-Induced Angina in a Myocardial Ischaemia-Reperfusion Injury Model
abstract	Percutaneous coronary intervention (PCI) effectively treats obstructive coronary artery syndrome. However, 30–40% patients continue to have angina after a successful PCI, thereby reducing patient satisfaction. The mechanisms underlying persistent angina after revascularisation therapy are still poorly understood; hence, the treatment or guideline for post-PCI angina remains unestablished. Thus, this study aimed to investigate the mechanisms underlying effort angina in animals following myocardial ischaemia-reperfusion (I/R) injury. Phosphorylated extracellular signal-regulated kinase (p-ERK), a marker for painful stimulation-induced neuronal activation, was used for the investigation. After a forced treadmill exercise (FTE), the number of p-ERK-expressing neurons increased in the superficial dorsal horn of the I/R model animals. Moreover, FTE evoked hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) production in the I/R-injured heart, inducing angina through TRPA1 activation on cardiac sensory fibres. Notably, the treatment of a TEMPOL, a reactive oxygen species scavenger, or TRPA1<sup<−/−</sup< mice successfully alleviated the FTE-induced p-ERK expression in the dorsal horn. The production of H<sub<2</sub<O<sub<2</sub<, a reactive oxygen species, through physical exercise contributes to angina development following I/R. Hence, our findings may be useful for understanding and treating angina following revascularisation therapy.
abstractGer	Percutaneous coronary intervention (PCI) effectively treats obstructive coronary artery syndrome. However, 30–40% patients continue to have angina after a successful PCI, thereby reducing patient satisfaction. The mechanisms underlying persistent angina after revascularisation therapy are still poorly understood; hence, the treatment or guideline for post-PCI angina remains unestablished. Thus, this study aimed to investigate the mechanisms underlying effort angina in animals following myocardial ischaemia-reperfusion (I/R) injury. Phosphorylated extracellular signal-regulated kinase (p-ERK), a marker for painful stimulation-induced neuronal activation, was used for the investigation. After a forced treadmill exercise (FTE), the number of p-ERK-expressing neurons increased in the superficial dorsal horn of the I/R model animals. Moreover, FTE evoked hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) production in the I/R-injured heart, inducing angina through TRPA1 activation on cardiac sensory fibres. Notably, the treatment of a TEMPOL, a reactive oxygen species scavenger, or TRPA1<sup<−/−</sup< mice successfully alleviated the FTE-induced p-ERK expression in the dorsal horn. The production of H<sub<2</sub<O<sub<2</sub<, a reactive oxygen species, through physical exercise contributes to angina development following I/R. Hence, our findings may be useful for understanding and treating angina following revascularisation therapy.
abstract_unstemmed	Percutaneous coronary intervention (PCI) effectively treats obstructive coronary artery syndrome. However, 30–40% patients continue to have angina after a successful PCI, thereby reducing patient satisfaction. The mechanisms underlying persistent angina after revascularisation therapy are still poorly understood; hence, the treatment or guideline for post-PCI angina remains unestablished. Thus, this study aimed to investigate the mechanisms underlying effort angina in animals following myocardial ischaemia-reperfusion (I/R) injury. Phosphorylated extracellular signal-regulated kinase (p-ERK), a marker for painful stimulation-induced neuronal activation, was used for the investigation. After a forced treadmill exercise (FTE), the number of p-ERK-expressing neurons increased in the superficial dorsal horn of the I/R model animals. Moreover, FTE evoked hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) production in the I/R-injured heart, inducing angina through TRPA1 activation on cardiac sensory fibres. Notably, the treatment of a TEMPOL, a reactive oxygen species scavenger, or TRPA1<sup<−/−</sup< mice successfully alleviated the FTE-induced p-ERK expression in the dorsal horn. The production of H<sub<2</sub<O<sub<2</sub<, a reactive oxygen species, through physical exercise contributes to angina development following I/R. Hence, our findings may be useful for understanding and treating angina following revascularisation therapy.
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title_short	Reactive Oxygen Species Cause Exercise-Induced Angina in a Myocardial Ischaemia-Reperfusion Injury Model
url	https://doi.org/10.3390/ijms23052820 https://doaj.org/article/d6507877de4d49539274d9c7a150121e https://www.mdpi.com/1422-0067/23/5/2820 https://doaj.org/toc/1661-6596 https://doaj.org/toc/1422-0067
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