期刊
TRENDS IN MOLECULAR MEDICINE
卷 25, 期 1, 页码 47-63出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2018.10.007
关键词
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资金
- Marie Curie Career Development Fellowship [275767]
- World Cancer Research grant [15-0228]
- ERC Advanced grant [323040]
Cell death is intrinsically linked to inflammatory liver disease and cancer development. Recent genetic studies have suggested that receptor-interacting protein kinase (RIPK) 1 is implicated in liver disease pathogenesis by regulating caspase-dependent hepatocyte apoptosis induced by tumor necrosis factor (TNF) or other stimuli. In contrast, the contribution of caspase-independent RIPK3/mixed lineage kinase like (MLKL)-mediated hepatocyte necroptosis remains debatable. Hepatocyte apoptosis depends on the balance between RIPK1 prosurvival scaffolding functions and its kinase-activity-mediated proapoptotic function. Several regulatory steps promote the prosurvival role of RIPK1, including phosphorylation and ubiquitination of RIPK1 itself and other molecules involved in RIPK1 signaling. Pharmacological inhibition of liver damage by targeting RIPK1 signaling emerges as a potential therapeutic strategy to prevent chronic liver inflammation and hepatocarcinogenesis.
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