CD36-Mediated Fatty Acid Oxidation in Hematopoietic Stem Cells Is a Novel Mechanism of Emergency Hematopoiesis in Response to Infection-Immunometabolism-CSCIED科技核心评价数据库-手机版

CD36-Mediated Fatty Acid Oxidation in Hematopoietic Stem Cells Is a Novel Mechanism of Emergency Hematopoiesis in Response to Infection

CD36-Mediated Fatty Acid Oxidation in Hematopoietic Stem Cells Is a Novel Mechanism of Emergency Hematopoiesis in Response to Infection

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DOI	10.20900/immunometab20220008
刊名	Immunometabolism IJ
年，卷(期)	2022, 4(2)
作者	Maryanovich, Maria; Ito, Keisuke,
作者单位	[Maryanovich, Maria; Ito, Keisuke] Albert Einstein Coll Med, Ruth L & David S Gottesman Inst Stem Cell & Regene, Bronx, NY 10461 USA; [Maryanovich, Maria; Ito, Keisuke] Albert Einstein Coll Med, Dept Cell Biol, Bronx, NY 10461 USA; It
摘要	Hematopoietic homeostasis depends on the close regulation of hematopoietic stem cell (HSC) activity in the bone marrow. Quiescence and activation in response to stress, among other changes in state, are mediated by shifts in HSC metabolic activity. Although HSC steady-state metabolism is well established, the mechanisms driving HSC activation, proliferation, and differentiation in response to stress remain poorly understood. Here we discuss a study by Mistry et al. that describes a novel metabolic mechanism that fuels HSC activation and expansion. The authors show that to meet their metabolic needs in response to infection, hematopoietic stem and progenitor cells uptake free fatty acids from their microenvironment via CD36 to fuel fatty acid oxidation. These exciting findings suggest that in the context of infection, HSCs undergo a metabolic shift toward fatty acid metabolism that drives emergency hematopoiesis and raise questions about the role of the microenvironment in this process.
Abstract	Hematopoietic homeostasis depends on the close regulation of hematopoietic stem cell (HSC) activity in the bone marrow. Quiescence and activation in response to stress, among other changes in state, are mediated by shifts in HSC metabolic activity. Although HSC steady-state metabolism is well established, the mechanisms driving HSC activation, proliferation, and differentiation in response to stress remain poorly understood. Here we discuss a study by Mistry et al. that describes a novel metabolic mechanism that fuels HSC activation and expansion. The authors show that to meet their metabolic needs in response to infection, hematopoietic stem and progenitor cells uptake free fatty acids from their microenvironment via CD36 to fuel fatty acid oxidation. These exciting findings suggest that in the context of infection, HSCs undergo a metabolic shift toward fatty acid metabolism that drives emergency hematopoiesis and raise questions about the role of the microenvironment in this process.
关键词	hematopoietic stem cells; infection; fatty-acid oxidation; CD36; oxidative phosphorylation; hematopoiesis
KeyWord	hematopoietic stem cells; infection; fatty-acid oxidation; CD36; oxidative phosphorylation; hematopoiesis
基金项目
页码	1-7

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Maryanovich, Maria; Ito, Keisuke. CD36-Mediated Fatty Acid Oxidation in Hematopoietic Stem Cells Is a Novel Mechanism of Emergency Hematopoiesis in Response to Infection [J]. Immunometabolism. 2022; 4; (2). 1 - 7.

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