Gutenberg Open Science: ACE inhibition modulates myeloid hematopoiesis after acute myocardial infarction and reduces cardiac and vascular inflammation in ischemic heart failure

Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-6210

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DC Field	Value	Language
dc.contributor.author	Rudi, Wolf-Stephan	-
dc.contributor.author	Molitor, Michael	-
dc.contributor.author	Garlapati, Venkata	-
dc.contributor.author	Finger, Stefanie	-
dc.contributor.author	Wild, Johannes	-
dc.contributor.author	Münzel, Thomas	-
dc.contributor.author	Karbach, Susanne H.	-
dc.contributor.author	Wenzel, Philip	-
dc.date.accessioned	2021-07-27T10:59:05Z	-
dc.date.available	2021-07-27T10:59:05Z	-
dc.date.issued	2021	-
dc.identifier.uri	https://openscience.ub.uni-mainz.de/handle/20.500.12030/6219	-
dc.description.abstract	Aims: Angiotensin-converting-enzyme inhibitors (ACE inhibitors) are a cornerstone of drug therapy after myocardial infarction (MI) and improve left ventricular function and survival. We aimed to elucidate the impact of early treatment with the ACE inhibitor ramipril on the hematopoietic response after MI, as well as on the chronic systemic and vascular inflammation. Methods and Results: In a mouse model of MI, induced by permanent ligation of the left anterior descending artery, immediate initiation of treatment with ramipril (10 mg/k/d via drinking water) reduced cardiac inflammation and the number of circulating inflammatory monocytes, whereas left ventricular function was not altered significantly, respectively. This effect was accompanied by enhanced retention of hematopoietic stem cells, Lin−Sca1−c-Kit+CD34+CD16/32+ granulocyte–macrophage progenitors (GMP) and Lin−Sca1−c-Kit+CD150−CD48− multipotent progenitors (MPP) in the bone marrow, with an upregulation of the niche factors Angiopoetin 1 and Kitl at 7 d post MI. Long-term ACE inhibition for 28 d limited vascular inflammation, particularly the infiltration of Ly6Chigh monocytes/macrophages, and reduced superoxide formation, resulting in improved endothelial function in mice with ischemic heart failure. Conclusion: ACE inhibition modulates the myeloid inflammatory response after MI due to the retention of myeloid precursor cells in their bone marrow reservoir. This results in a reduction in cardiac and vascular inflammation with improvement in survival after MI.	en_GB
dc.description.sponsorship	Open Access-Publizieren Universität Mainz / Universitätsmedizin Mainz	de
dc.language.iso	eng	de
dc.rights	CC BY	*
dc.rights.uri	https://creativecommons.org/licenses/by/4.0/	*
dc.subject.ddc	610 Medizin	de_DE
dc.subject.ddc	610 Medical sciences	en_GB
dc.title	ACE inhibition modulates myeloid hematopoiesis after acute myocardial infarction and reduces cardiac and vascular inflammation in ischemic heart failure	en_GB
dc.type	Zeitschriftenaufsatz	de
dc.identifier.doi	http://doi.org/10.25358/openscience-6210	-
jgu.type.dinitype	article	en_GB
jgu.type.version	Published version	de
jgu.type.resource	Text	de
jgu.organisation.department	FB 04 Medizin	de
jgu.organisation.number	2700	-
jgu.organisation.name	Johannes Gutenberg-Universität Mainz	-
jgu.rights.accessrights	openAccess	-
jgu.journal.title	Antioxidants	de
jgu.journal.volume	10	de
jgu.journal.issue	3	de
jgu.pages.alternative	396	de
jgu.publisher.year	2021	-
jgu.publisher.name	MDPI	de
jgu.publisher.place	Basel	de
jgu.publisher.uri	https://doi.org/10.3390/antiox10030396	de
jgu.publisher.issn	2076-3921	de
jgu.organisation.place	Mainz	-
jgu.subject.ddccode	610	de
jgu.publisher.doi	10.3390/antiox10030396
jgu.organisation.ror	https://ror.org/023b0x485
Appears in collections:	JGU-Publikationen

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