Innate and adaptive immune responses subsequent to ischemia-reperfusion injury in the kidney.

No abstract is available for this paper.

• Publication year

  2014

• Venue

  Progrès en urologie (Paris)

• Publication date

  2014-06-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/S1166-7087(14)70058-2PMID 24950927
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Cell Death

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• Cell death.

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• Hepatic Ischemia/Reperfusion Injury Involves Functional TLR4 Signaling in Nonparenchymal Cells1

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• Identification of thrombospondin 1 (TSP-1) as a novel mediator of cell injury in kidney ischemia.

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• Toll‐Like Receptor and Heme Oxygenase‐1 Signaling in Hepatic Ischemia/Reperfusion Injury

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• A2A Adenosine Receptors on Bone Marrow-Derived Cells Protect Liver from Ischemia-Reperfusion Injury1

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• Persistent renal and extrarenal immune changes after severe ischemic injury.

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• Renal-associated TLR2 mediates ischemia/reperfusion injury in the kidney.

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• The mannose-binding lectin-pathway is involved in complement activation in the course of renal ischemia-reperfusion injury.

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