期刊
PHARMACOLOGICAL RESEARCH
卷 128, 期 -, 页码 88-100出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.phrs.2017.10.001
关键词
AMP-activated protein kinase; Janus kinase; Rheumatoid arthritis; Myeloproliferative neoplasms; Lymphoma
资金
- British Heart Foundation [PG/12/1/29276, PG/13/82/30483, PG/14/32/30812]
- Chief Scientist Office [ETM/226]
- NHS Greater Glasgow and Clyde Research Endowment Fund [2011REFCH08]
- Chest, Heart and Stroke Scotland [R10/A131]
- Diabetes UK [BDA11/0004309, BDA11/0004403]
- British Heart Foundation [PG/12/1/29276, PG/14/32/30812, PG/13/82/30483] Funding Source: researchfish
- Chief Scientist Office [ETM/226] Funding Source: researchfish
Exaggerated Janus kinase-signal transducer and activator of transcription (JAK-STAT) signalling is key to the pathogenesis of pro-inflammatory disorders, such as rheumatoid arthritis and cardiovascular diseases. Mutational activation of JAKs is also responsible for several haematological malignancies, including myeloproliferative neoplasms and acute lymphoblastic leukaemia. Accumulating evidence links adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK), an energy sensor and regulator of organismal and cellular metabolism, with the suppression of immune and inflammatory processes. Recent studies have shown that activation of AMPK can limit JAK-STAT-dependent signalling pathways via several mechanisms. These novel findings support AMPK activation as a strategy for management of an array of disorders characterised by hyper-activation of the JAK-STAT pathway. This review discusses the pivotal role of JAK-STAT signalling in a range of disorders and how both established clinically used and novel AMPK activators might be used to treat these conditions. (C) 2017 Elsevier Ltd. All rights reserved.
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