% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Dellorusso:294551,
      author       = {P. V. Dellorusso and M. A. Proven and F. J. Calero-Nieto
                      and X. Wang and C. A. Mitchell and F. Hartmann$^*$ and M.
                      Amouzgar and P. Favaro and A. DeVilbiss and J. W. Swann and
                      T. T. Ho and Z. Zhao and S. C. Bendall and S. Morrison and
                      B. Göttgens and E. Passegué},
      title        = {{A}utophagy counters inflammation-driven glycolytic
                      impairment in aging hematopoietic stem cells.},
      journal      = {Cell stem cell},
      volume       = {31},
      number       = {7},
      issn         = {1934-5909},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2024-02326},
      pages        = {1020 - 1037.e9},
      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.},
      keywords     = {Animals / Autophagy / Hematopoietic Stem Cells: metabolism
                      / Inflammation: pathology / Inflammation: metabolism /
                      Glycolysis / Mice / Mice, Inbred C57BL / Aging: pathology /
                      Aging: metabolism / Cellular Senescence / Signal
                      Transduction / Suppressor of Cytokine Signaling 3 Protein:
                      metabolism / Glucose: metabolism / aging (Other) / autophagy
                      (Other) / hematopoietic stem cells (Other) / inflammation
                      (Other) / metabolism (Other) / regeneration (Other) /
                      Suppressor of Cytokine Signaling 3 Protein (NLM Chemicals) /
                      Glucose (NLM Chemicals)},
      ddc          = {570},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38754428},
      pmc          = {pmc:PMC11350610},
      doi          = {10.1016/j.stem.2024.04.020},
      url          = {https://inrepo02.dkfz.de/record/294551},
}