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000294551 0247_ $$2doi$$a10.1016/j.stem.2024.04.020
000294551 0247_ $$2pmid$$apmid:38754428
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000294551 0247_ $$2ISSN$$a1875-9777
000294551 037__ $$aDKFZ-2024-02326
000294551 041__ $$aEnglish
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000294551 1001_ $$aDellorusso, Paul V$$b0
000294551 245__ $$aAutophagy counters inflammation-driven glycolytic impairment in aging hematopoietic stem cells.
000294551 260__ $$aAmsterdam [u.a.]$$bElsevier$$c2024
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000294551 520__ $$aAutophagy is central to the benefits of longevity signaling programs and to hematopoietic stem cell (HSC) response to nutrient stress. With age, a subset of HSCs increases autophagy flux and preserves regenerative capacity, but the signals triggering autophagy and maintaining the functionality of autophagy-activated old HSCs (oHSCs) remain unknown. Here, we demonstrate that autophagy is an adaptive cytoprotective response to chronic inflammation in the aging murine bone marrow (BM) niche. We find that inflammation impairs glucose uptake and suppresses glycolysis in oHSCs through Socs3-mediated inhibition of AKT/FoxO-dependent signaling, with inflammation-mediated autophagy engagement preserving functional quiescence by enabling metabolic adaptation to glycolytic impairment. Moreover, we show that transient autophagy induction via a short-term fasting/refeeding paradigm normalizes glycolytic flux and significantly boosts oHSC regenerative potential. Our results identify inflammation-driven glucose hypometabolism as a key driver of HSC dysfunction with age and establish autophagy as a targetable node to reset oHSC regenerative capacity.
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000294551 650_7 $$2Other$$aaging
000294551 650_7 $$2Other$$aautophagy
000294551 650_7 $$2Other$$ahematopoietic stem cells
000294551 650_7 $$2Other$$ainflammation
000294551 650_7 $$2Other$$ametabolism
000294551 650_7 $$2Other$$aregeneration
000294551 650_7 $$2NLM Chemicals$$aSuppressor of Cytokine Signaling 3 Protein
000294551 650_7 $$0IY9XDZ35W2$$2NLM Chemicals$$aGlucose
000294551 650_2 $$2MeSH$$aAnimals
000294551 650_2 $$2MeSH$$aAutophagy
000294551 650_2 $$2MeSH$$aHematopoietic Stem Cells: metabolism
000294551 650_2 $$2MeSH$$aInflammation: pathology
000294551 650_2 $$2MeSH$$aInflammation: metabolism
000294551 650_2 $$2MeSH$$aGlycolysis
000294551 650_2 $$2MeSH$$aMice
000294551 650_2 $$2MeSH$$aMice, Inbred C57BL
000294551 650_2 $$2MeSH$$aAging: pathology
000294551 650_2 $$2MeSH$$aAging: metabolism
000294551 650_2 $$2MeSH$$aCellular Senescence
000294551 650_2 $$2MeSH$$aSignal Transduction
000294551 650_2 $$2MeSH$$aSuppressor of Cytokine Signaling 3 Protein: metabolism
000294551 650_2 $$2MeSH$$aGlucose: metabolism
000294551 7001_ $$aProven, Melissa A$$b1
000294551 7001_ $$aCalero-Nieto, Fernando J$$b2
000294551 7001_ $$aWang, Xiaonan$$b3
000294551 7001_ $$aMitchell, Carl A$$b4
000294551 7001_ $$0P:(DE-He78)5cbf51db82a42b08a814f47dbc9412ca$$aHartmann, Felix$$b5$$udkfz
000294551 7001_ $$aAmouzgar, Meelad$$b6
000294551 7001_ $$aFavaro, Patricia$$b7
000294551 7001_ $$aDeVilbiss, Andrew$$b8
000294551 7001_ $$aSwann, James W$$b9
000294551 7001_ $$aHo, Theodore T$$b10
000294551 7001_ $$aZhao, Zhiyu$$b11
000294551 7001_ $$aBendall, Sean C$$b12
000294551 7001_ $$aMorrison, Sean$$b13
000294551 7001_ $$aGöttgens, Berthold$$b14
000294551 7001_ $$aPassegué, Emmanuelle$$b15
000294551 773__ $$0PERI:(DE-600)2375356-0$$a10.1016/j.stem.2024.04.020$$gVol. 31, no. 7, p. 1020 - 1037.e9$$n7$$p1020 - 1037.e9$$tCell stem cell$$v31$$x1934-5909$$y2024
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