Protective role of c-Jun N-terminal kinase 2 in acetaminophen-induced liver injury
Protective role of c-Jun N-terminal kinase 2 in acetaminophen-induced liver injury
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DOI：
10.1016/j.bbrc.2008.06.065
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发表时间：
2008-09-12
影响因子：
3.1
通讯作者：
Pohl, Lance R.
中科院分区：
文献类型：
--
作者：
Bourdi, Mohammed;Korrapati, Midhun C.;Pohl, Lance R.
Recent studies in mice suggest that stress-activated c-Jun N-terminal protein kinase 2 (JNK2) plays a pathologic role in acetaminophen (APAP)-induced liver injury (AILI), a major cause of acute liver failure (ALF). In contrast, we present evidence that JNK2 can have a protective role against AILI When male C57BL/6J wild type (WT) and JNK2(-/-) mice were treated with 300 mg APAP/kg, 90% of JNK2(-/-) mice died of ALF compared to 20% of WT mice within 48 h. The high susceptibility of JNK2(-/-) mice to AILI appears to be due in part to deficiencies in hepatocyte proliferation and repair. Therefore, our findings are consistent with JNK2 signaling playing a protective role in AILI and further suggest that the use of JNK inhibitors as a potential treatment for AILI as has been recommended by other investigators, should be reconsidered. Published by Elsevier Inc.
