Quo Vadis? Immunodynamics of Myeloid Cells after Myocardial Infarction

Myocardial infarction (MI), a major contributor to worldwide morbidity and mortality, is caused by a lack of blood flow to the heart. Affected heart tissue becomes ischemic due to deficiency of blood perfusion and oxygen delivery. In case sufficient blood flow cannot be timely restored, cardiac inju...
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Autor*in:	Aldo Moggio [verfasserIn] Heribert Schunkert [verfasserIn] Thorsten Kessler [verfasserIn] Hendrik B. Sager [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	myocardial infarction hematopoiesis myeloid cells extracellular signaling inflammation cellular heterogeneity

Übergeordnetes Werk:	In: International Journal of Molecular Sciences - MDPI AG, 2003, 23(2022), 24, p 15814
Übergeordnetes Werk:	volume:23 ; year:2022 ; number:24, p 15814

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

DOI / URN:	10.3390/ijms232415814

Katalog-ID:	DOAJ083147535

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520			\|a Myocardial infarction (MI), a major contributor to worldwide morbidity and mortality, is caused by a lack of blood flow to the heart. Affected heart tissue becomes ischemic due to deficiency of blood perfusion and oxygen delivery. In case sufficient blood flow cannot be timely restored, cardiac injury with necrosis occurs. The ischemic/necrotic area induces a systemic inflammatory response and hundreds of thousands of leukocytes are recruited from the blood to the injured heart. The blood pool of leukocytes is rapidly depleted and urgent re-supply of these cells is needed. Myeloid cells are generated in the bone marrow (BM) and spleen, released into the blood, travel to sites of need, extravasate and accumulate inside tissues to accomplish various functions. In this review we focus on the “leukocyte supply chain” and will separately evaluate different myeloid cell compartments (BM, spleen, blood, heart) in steady state and after MI. Moreover, we highlight the local and systemic kinetics of extracellular factors, chemokines and danger signals involved in the regulation of production/generation, release, transportation, uptake, and activation of myeloid cells during the inflammatory phase of MI.
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language	English
source	In International Journal of Molecular Sciences 23(2022), 24, p 15814 volume:23 year:2022 number:24, p 15814
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callnumber-first	Q - Science
author	Aldo Moggio
spellingShingle	Aldo Moggio misc QH301-705.5 misc QD1-999 misc myocardial infarction misc hematopoiesis misc myeloid cells misc extracellular signaling misc inflammation misc cellular heterogeneity misc Biology (General) misc Chemistry Quo Vadis? Immunodynamics of Myeloid Cells after Myocardial Infarction
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topic_title	QH301-705.5 QD1-999 Quo Vadis? Immunodynamics of Myeloid Cells after Myocardial Infarction myocardial infarction hematopoiesis myeloid cells extracellular signaling inflammation cellular heterogeneity
topic	misc QH301-705.5 misc QD1-999 misc myocardial infarction misc hematopoiesis misc myeloid cells misc extracellular signaling misc inflammation misc cellular heterogeneity misc Biology (General) misc Chemistry
topic_unstemmed	misc QH301-705.5 misc QD1-999 misc myocardial infarction misc hematopoiesis misc myeloid cells misc extracellular signaling misc inflammation misc cellular heterogeneity misc Biology (General) misc Chemistry
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title	Quo Vadis? Immunodynamics of Myeloid Cells after Myocardial Infarction
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title_sort	quo vadis? immunodynamics of myeloid cells after myocardial infarction
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title_auth	Quo Vadis? Immunodynamics of Myeloid Cells after Myocardial Infarction
abstract	Myocardial infarction (MI), a major contributor to worldwide morbidity and mortality, is caused by a lack of blood flow to the heart. Affected heart tissue becomes ischemic due to deficiency of blood perfusion and oxygen delivery. In case sufficient blood flow cannot be timely restored, cardiac injury with necrosis occurs. The ischemic/necrotic area induces a systemic inflammatory response and hundreds of thousands of leukocytes are recruited from the blood to the injured heart. The blood pool of leukocytes is rapidly depleted and urgent re-supply of these cells is needed. Myeloid cells are generated in the bone marrow (BM) and spleen, released into the blood, travel to sites of need, extravasate and accumulate inside tissues to accomplish various functions. In this review we focus on the “leukocyte supply chain” and will separately evaluate different myeloid cell compartments (BM, spleen, blood, heart) in steady state and after MI. Moreover, we highlight the local and systemic kinetics of extracellular factors, chemokines and danger signals involved in the regulation of production/generation, release, transportation, uptake, and activation of myeloid cells during the inflammatory phase of MI.
abstractGer	Myocardial infarction (MI), a major contributor to worldwide morbidity and mortality, is caused by a lack of blood flow to the heart. Affected heart tissue becomes ischemic due to deficiency of blood perfusion and oxygen delivery. In case sufficient blood flow cannot be timely restored, cardiac injury with necrosis occurs. The ischemic/necrotic area induces a systemic inflammatory response and hundreds of thousands of leukocytes are recruited from the blood to the injured heart. The blood pool of leukocytes is rapidly depleted and urgent re-supply of these cells is needed. Myeloid cells are generated in the bone marrow (BM) and spleen, released into the blood, travel to sites of need, extravasate and accumulate inside tissues to accomplish various functions. In this review we focus on the “leukocyte supply chain” and will separately evaluate different myeloid cell compartments (BM, spleen, blood, heart) in steady state and after MI. Moreover, we highlight the local and systemic kinetics of extracellular factors, chemokines and danger signals involved in the regulation of production/generation, release, transportation, uptake, and activation of myeloid cells during the inflammatory phase of MI.
abstract_unstemmed	Myocardial infarction (MI), a major contributor to worldwide morbidity and mortality, is caused by a lack of blood flow to the heart. Affected heart tissue becomes ischemic due to deficiency of blood perfusion and oxygen delivery. In case sufficient blood flow cannot be timely restored, cardiac injury with necrosis occurs. The ischemic/necrotic area induces a systemic inflammatory response and hundreds of thousands of leukocytes are recruited from the blood to the injured heart. The blood pool of leukocytes is rapidly depleted and urgent re-supply of these cells is needed. Myeloid cells are generated in the bone marrow (BM) and spleen, released into the blood, travel to sites of need, extravasate and accumulate inside tissues to accomplish various functions. In this review we focus on the “leukocyte supply chain” and will separately evaluate different myeloid cell compartments (BM, spleen, blood, heart) in steady state and after MI. Moreover, we highlight the local and systemic kinetics of extracellular factors, chemokines and danger signals involved in the regulation of production/generation, release, transportation, uptake, and activation of myeloid cells during the inflammatory phase of MI.
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title_short	Quo Vadis? Immunodynamics of Myeloid Cells after Myocardial Infarction
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