Platelets mediate acetaminophen hepatotoxicity

Blood. 2015 Oct 8;126(15):1738-9. doi: 10.1182/blood-2015-07-659516.


In this issue of Blood, Miyakawa et al show that platelets and protease-activated receptor (PAR)-4 contribute to acetaminophen (APAP)-induced liver damage. Using various strategies in a mouse model of APAP overdose, the authors demonstrate that platelets participate in the progression of liver damage, and that the direct thrombin inhibitor lepirudin and PAR-4 deficiency attenuate hepatotoxicity. These findings have the potential to help identify future therapeutic targets for APAP-induced hepatotoxicity.

Publication types

  • Comment

MeSH terms

  • Acetaminophen / toxicity*
  • Animals
  • Antithrombin III / metabolism*
  • Blood Platelets / pathology*
  • Chemical and Drug Induced Liver Injury / etiology*
  • Hematopoietic Stem Cells / drug effects*
  • Hepatocytes / drug effects*
  • Male
  • Peptide Hydrolases / metabolism*
  • Receptors, Proteinase-Activated / physiology*


  • Receptors, Proteinase-Activated
  • Acetaminophen
  • Antithrombin III
  • Peptide Hydrolases