articleProceedings of the National Academy of SciencesNov 10, 2014BRONZE OA

Synchronized renal tubular cell death involves ferroptosis

ALAndreas LinkermannRSRachid SkoutaNHNina HimmerkusSRShrikant R. MulayCDChristin Dewitz

Christian-Albrechts-Universität zu Kiel · The University of Texas at El Paso · +14 more institutions

PubMed
Indexed incrossrefdatacitepubmed

Abstract

Receptor-interacting protein kinase 3 (RIPK3)-mediated necroptosis is thought to be the pathophysiologically predominant pathway that leads to regulated necrosis of parenchymal cells in ischemia-reperfusion injury (IRI), and loss of either Fas-associated protein with death domain (FADD) or caspase-8 is known to sensitize tissues to undergo spontaneous necroptosis. Here, we demonstrate that renal tubules do not undergo sensitization to necroptosis upon genetic ablation of either FADD or caspase-8 and that the RIPK1 inhibitor necrostatin-1 (Nec-1) does not protect freshly isolated tubules from hypoxic injury. In contrast, iron-dependent ferroptosis directly causes synchronized necrosis of renal tubules, as…

Citation impact

1,096
total citations
FWCI
30.78
Percentile
100%
References
38
Citations per year

Authors

23

Topics & keywords

Topics
Keywords
  • Necrosis
  • Programmed cell death
  • Ischemia
  • Sepsis
  • Medicine
  • Transplantation
  • Immune system
  • Myocardial infarction
UN Sustainable Development Goals
  • Good health and well-being
No related works found for this paper.

Funding