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@ARTICLE{Dellorusso1:294448,
      author       = {P. V. Dellorusso 1 and M. A. Proven 1 and F. J.
                      Calero-Nieto and X. W. and C. A. Mitchell and F. H. and M.
                      A. and P. F. and A. D. and J. W. Swann and T. T. Ho and Z.
                      Z. and S. C. Bendall and S. M. and B. G. and E. P. 1. 7.},
      title        = {{A}utophagy counters inflammation-driven glycolytic
                      impairment in aging hematopoietic stem cells},
      journal      = {Cell stem cell},
      volume       = {31},
      number       = {7},
      reportid     = {DKFZ-2024-02273},
      pages        = {1020-1037},
      year         = {2024},
      abstract     = {Autophagy 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.},
      cin          = {D260},
      cid          = {I:(DE-He78)D260-20160331},
      typ          = {PUB:(DE-HGF)16},
      doi          = {doi: 10.1016/j.stem.2024.04.020. },
      url          = {https://inrepo02.dkfz.de/record/294448},
}