Hartmut Jaeschke
University of Kansas
453 Papers
3.7K Citations
Hartmut Jaeschke is an academic researcher from University of Kansas. The author has contributed to research in topics: Liver injury & Acetaminophen. The author has an hindex of 106, co-authored 424 publications. Previous affiliations of Hartmut Jaeschke include Baylor College of Medicine & University Medical Center New Orleans.
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Papers
Connexin32: a mediator of acetaminophen-induced liver injury?
Michaël Maes,Mitchell R. McGill,Tereza Cristina da Silva,Margitta Lebofsky,Cintia Maria Monteiro de Araújo,Taynã Tiburcio,Isabel Veloso Alves Pereira,Joost Willebrords,Sara Crespo Yanguas,Anwar Farhood,Maria Lúcia Zaidan Dagli,Hartmut Jaeschke,Bruno Cogliati,Mathieu Vinken +13 more
TL;DR: It was found that genetic ablation of connexin32 has no influence on several key events in acetaminophen-induced hepatotoxicity, including cell death, inflammation or oxidative stress, yet it does affect production of protein adducts as well as proliferating cell nuclear antigen steady-state protein levels.
Hepatitis C virus structural proteins can exacerbate or ameliorate acetaminophen-induced liver injury in mice
TL;DR: While HCV infection could exacerbate APAP-induced liver injury due to induction and amplification of mitochondrial oxidant stress, it could also protect against injury by activation of APAP scavenging mechanisms.
Critical Factors in the Assessment of Cholestatic Liver Injury In Vitro.
TL;DR: This chapter focuses on the establishment of a system for determining the effects of cholestatic concentrations of bile acids on hepatocytes using primary hepatocytes or hepatoma cell lines and the response of different species to bile acid exposure.
Impaired protein adduct removal following repeat administration of subtoxic doses of acetaminophen enhances liver injury in fed mice
Nga T. Nguyen,Jephte Y. Akakpo,James L. Weemhoff,Anup Ramachandran,Wen-Xing Ding,Hartmut Jaeschke +5 more
TL;DR: In this article, the role of autophagy in APAP-induced liver injury after multiple subtoxic doses was examined and the importance of adaptive responses such as autophagia in removing protein adducts and preventing liver injury was highlighted.
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The role of the c-Jun N-terminal kinases 1/2 and receptor-interacting protein kinase 3 in furosemide-induced liver injury.
TL;DR: Data show that, although JNK activation and RIP3 expression are induced by FS, neither contributes to the liver injury.
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