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@ARTICLE{Galy:284407,
      author       = {B. Galy$^*$ and M. Conrad and M. Muckenthaler},
      title        = {{M}echanisms controlling cellular and systemic iron
                      homeostasis.},
      journal      = {Nature reviews},
      volume       = {25},
      number       = {2},
      issn         = {1471-0072},
      address      = {London},
      publisher    = {Macmillan},
      reportid     = {DKFZ-2023-01996},
      pages        = {133-155},
      year         = {2024},
      note         = {#EA:F170# / 2024 Feb;25(2):133-155},
      abstract     = {In mammals, hundreds of proteins use iron in a multitude of
                      cellular functions, including vital processes such as
                      mitochondrial respiration, gene regulation and DNA synthesis
                      or repair. Highly orchestrated regulatory systems control
                      cellular and systemic iron fluxes ensuring sufficient iron
                      delivery to target proteins is maintained, while limiting
                      its potentially deleterious effects in iron-mediated
                      oxidative cell damage and ferroptosis. In this Review, we
                      discuss how cells acquire, traffick and export iron and how
                      stored iron is mobilized for iron-sulfur cluster and haem
                      biogenesis. Furthermore, we describe how these cellular
                      processes are fine-tuned by the combination of various
                      sensory and regulatory systems, such as the iron-regulatory
                      protein (IRP)-iron-responsive element (IRE) network, the
                      nuclear receptor co-activator 4 (NCOA4)-mediated
                      ferritinophagy pathway, the prolyl hydroxylase domain
                      (PHD)-hypoxia-inducible factor (HIF) axis or the nuclear
                      factor erythroid 2-related factor 2 (NRF2) regulatory hub.
                      We further describe how these pathways interact with
                      systemic iron homeostasis control through the
                      hepcidin-ferroportin axis to ensure appropriate iron fluxes.
                      This knowledge is key for the identification of novel
                      therapeutic opportunities to prevent diseases of cellular
                      and/or systemic iron mismanagement.},
      subtyp        = {Review Article},
      cin          = {F170},
      ddc          = {570},
      cid          = {I:(DE-He78)F170-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37783783},
      doi          = {10.1038/s41580-023-00648-1},
      url          = {https://inrepo02.dkfz.de/record/284407},
}