title: Platelets mediate acetaminophen hepatotoxicity.
abstract: 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.
authors.affiliation: MICHAEL E. DeBAKEY VA MEDICAL CENTER; BAYLOR COLLEGE OF MEDICINE.
authors.forename: Fong W
authors.initials: FW
authors.lastname: Lam
authors.affiliation: MICHAEL E. DeBAKEY VA MEDICAL CENTER; BAYLOR COLLEGE OF MEDICINE.
authors.forename: Rolando E
authors.initials: RE
authors.lastname: Rumbaut
mesh_terms: D000082:Acetaminophen / Q000633:toxicity*; D000818:Animals; D000990:Antithrombin III / Q000378:metabolism*; D001792:Blood Platelets / Q000473:pathology*; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology*; D006412:Hematopoietic Stem Cells / Q000187:drug effects*; D022781:Hepatocytes / Q000187:drug effects*; D008297:Male; D010447:Peptide Hydrolases / Q000378:metabolism*; D044462:Receptors, Proteinase-Activated / Q000502:physiology*
chemical_list: D044462:Receptors, Proteinase-Activated; D000082:Acetaminophen; D000990:Antithrombin III; D010447:Peptide Hydrolases