Nature Communications (Feb 2022)

Targeting ferroptosis protects against experimental (multi)organ dysfunction and death

  • Samya Van Coillie,
  • Emily Van San,
  • Ines Goetschalckx,
  • Bartosz Wiernicki,
  • Banibrata Mukhopadhyay,
  • Wulf Tonnus,
  • Sze Men Choi,
  • Ria Roelandt,
  • Catalina Dumitrascu,
  • Ludwig Lamberts,
  • Geert Dams,
  • Wannes Weyts,
  • Jelle Huysentruyt,
  • Behrouz Hassannia,
  • Irina Ingold,
  • Suhas Lele,
  • Evelyne Meyer,
  • Maya Berg,
  • Ruth Seurinck,
  • Yvan Saeys,
  • An Vermeulen,
  • Alexander L. N. van Nuijs,
  • Marcus Conrad,
  • Andreas Linkermann,
  • Mohan Rajapurkar,
  • Peter Vandenabeele,
  • Eric Hoste,
  • Koen Augustyns,
  • Tom Vanden Berghe

DOI
https://doi.org/10.1038/s41467-022-28718-6
Journal volume & issue
Vol. 13, no. 1
pp. 1 – 14

Abstract

Read online

Catalytic iron is associated with intensive care unit mortality and is known to cause free radical-mediated cellular toxicity. Here the authors show that a soluble ferrostatin-analogue (a ferroptosis inhibitor) protects mice from injury and death in experimental iron overload induced and genetic models of organ dysfunction, but not sepsis-induced multiorgan dysfunction.