Acute kidney injury: A conspiracy of toll-like receptor 4 on endothelia, leukocytes, and tubules

Christopher Y. Lu, Pamela D. Winterberg, Jianlin Chen, John R. Hartono

Research output: Contribution to journalReview article

20 Scopus citations


Ischemic acute kidney injury (AKI) contributes to considerable morbidity and mortality in hospitalized patients and can contribute to rejection during kidney transplantation. Maladaptive immune responses can exacerbate injury, and targeting these responses holds promise as therapy for AKI. In the last decade, a number of molecules and receptors were identified in the innate immune response to ischemia-reperfusion injury. This review primarily focuses on one pathway that leads to maladaptive inflammation: toll-like receptor 4 (TLR4) and one of its ligands, high mobility group box protein 1 (HMGB1). The temporal-spatial roles and potential therapeutics targeting this particular receptor-ligand interaction are also explored.

Original languageEnglish (US)
Pages (from-to)1847-1854
Number of pages8
JournalPediatric Nephrology
Issue number10
StatePublished - Oct 1 2012



  • Damage associated molecular patterns
  • Innate immunity
  • Ischemic acute kidney injury
  • Toll-like receptor
  • Transplant rejection

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Nephrology

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