Dynamics of angiogenesis in ischemic areas of the infarcted heart

Abstract Cardiomyocytes are susceptible to apoptosis caused by hypoxia during the acute and subacute phases of myocardial infarction (MI). Angiogenesis can reduce MI-induced damage by mitigating hypoxia. It has been speculated that the ischemic border zone is a unique area rescued by angiogenic ther...

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Autores principales:	Koichi Kobayashi, Kengo Maeda, Mikito Takefuji, Ryosuke Kikuchi, Yoshihiro Morishita, Masanori Hirashima, Toyoaki Murohara
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/043056593d774c23a939e6a0cb6307c8
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spelling	oai:doaj.org-article:043056593d774c23a939e6a0cb6307c82021-12-02T15:05:00ZDynamics of angiogenesis in ischemic areas of the infarcted heart10.1038/s41598-017-07524-x2045-2322https://doaj.org/article/043056593d774c23a939e6a0cb6307c82017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-07524-xhttps://doaj.org/toc/2045-2322Abstract Cardiomyocytes are susceptible to apoptosis caused by hypoxia during the acute and subacute phases of myocardial infarction (MI). Angiogenesis can reduce MI-induced damage by mitigating hypoxia. It has been speculated that the ischemic border zone is a unique area rescued by angiogenic therapy. However, the mechanism and timing for new vessel formation in the mammalian heart following hypoxia are unclear. Identifying targets that benefit from angiogenesis treatment is indispensable for the development of revolutionary therapies. Here, we describe a novel circulatory system wherein new vessels develop from the endocardium of the left ventricle to perfuse the hypoxic area and salvage damaged cardiomyocytes at 3–14 days after MI by activating vascular endothelial growth factor signaling. Moreover, enhanced angiogenesis increased cardiomyocyte survival along the endocardium in the ischemic zone and suppressed ventricular remodeling in infarcted hearts. In contrast, cardiomyocytes in the border zone’s hypoxic area underwent apoptosis within 12 h of MI, and the border area that was amenable to treatment disappeared. These data indicate that the non-perfused area along the endocardium is a site of active angiogenesis and a promising target for MI treatment.Koichi KobayashiKengo MaedaMikito TakefujiRyosuke KikuchiYoshihiro MorishitaMasanori HirashimaToyoaki MuroharaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Koichi Kobayashi Kengo Maeda Mikito Takefuji Ryosuke Kikuchi Yoshihiro Morishita Masanori Hirashima Toyoaki Murohara Dynamics of angiogenesis in ischemic areas of the infarcted heart
description	Abstract Cardiomyocytes are susceptible to apoptosis caused by hypoxia during the acute and subacute phases of myocardial infarction (MI). Angiogenesis can reduce MI-induced damage by mitigating hypoxia. It has been speculated that the ischemic border zone is a unique area rescued by angiogenic therapy. However, the mechanism and timing for new vessel formation in the mammalian heart following hypoxia are unclear. Identifying targets that benefit from angiogenesis treatment is indispensable for the development of revolutionary therapies. Here, we describe a novel circulatory system wherein new vessels develop from the endocardium of the left ventricle to perfuse the hypoxic area and salvage damaged cardiomyocytes at 3–14 days after MI by activating vascular endothelial growth factor signaling. Moreover, enhanced angiogenesis increased cardiomyocyte survival along the endocardium in the ischemic zone and suppressed ventricular remodeling in infarcted hearts. In contrast, cardiomyocytes in the border zone’s hypoxic area underwent apoptosis within 12 h of MI, and the border area that was amenable to treatment disappeared. These data indicate that the non-perfused area along the endocardium is a site of active angiogenesis and a promising target for MI treatment.
format	article
author	Koichi Kobayashi Kengo Maeda Mikito Takefuji Ryosuke Kikuchi Yoshihiro Morishita Masanori Hirashima Toyoaki Murohara
author_facet	Koichi Kobayashi Kengo Maeda Mikito Takefuji Ryosuke Kikuchi Yoshihiro Morishita Masanori Hirashima Toyoaki Murohara
author_sort	Koichi Kobayashi
title	Dynamics of angiogenesis in ischemic areas of the infarcted heart
title_short	Dynamics of angiogenesis in ischemic areas of the infarcted heart
title_full	Dynamics of angiogenesis in ischemic areas of the infarcted heart
title_fullStr	Dynamics of angiogenesis in ischemic areas of the infarcted heart
title_full_unstemmed	Dynamics of angiogenesis in ischemic areas of the infarcted heart
title_sort	dynamics of angiogenesis in ischemic areas of the infarcted heart
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/043056593d774c23a939e6a0cb6307c8
work_keys_str_mv	AT koichikobayashi dynamicsofangiogenesisinischemicareasoftheinfarctedheart AT kengomaeda dynamicsofangiogenesisinischemicareasoftheinfarctedheart AT mikitotakefuji dynamicsofangiogenesisinischemicareasoftheinfarctedheart AT ryosukekikuchi dynamicsofangiogenesisinischemicareasoftheinfarctedheart AT yoshihiromorishita dynamicsofangiogenesisinischemicareasoftheinfarctedheart AT masanorihirashima dynamicsofangiogenesisinischemicareasoftheinfarctedheart AT toyoakimurohara dynamicsofangiogenesisinischemicareasoftheinfarctedheart
_version_	1718388934106415104

Dynamics of angiogenesis in ischemic areas of the infarcted heart

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