期刊
JOURNAL OF MOLECULAR ENDOCRINOLOGY
卷 55, 期 2, 页码 R11-R22出版社
BIOSCIENTIFICA LTD
DOI: 10.1530/JME-15-0146
关键词
JNK; p38; SAPK; metabolism; obesity; stress; adipose tissue; brain and signal transduction
资金
- Principe de Girona award
- ERC [260464]
- MICINN [SAF2013-43506-R]
- Comunidad de Madrid [S2010/BMD-2326]
- Spanish Ministry of Economy and Competitiveness
- Pro-CNIC Foundation
- EFSD 2030
- European Research Council (ERC) [260464] Funding Source: European Research Council (ERC)
Obesity is a new global pandemic, with growing incidence and prevalence. This disease is associated with increased risk of several pathologies, including diabetes, cardiovascular diseases, and cancer. The mechanisms underlying obesity-associated metabolic changes are the focus of efforts to identify new therapies. Stress-activated protein kinases (SAPK), including cJun N-terminal kinases (JNKs) and p38, are required for cellular responses to metabolic stress and therefore might contribute to the pathogenesis of obesity. Tissue-specific knockout models support a cell-type-specific role for JNK isoforms, in particular JNK1, highlighting its importance in cell homeostasis and organ crosstalk. However, more efforts are needed to elucidate the specific roles of other JNK isoforms and p38 family members in metabolism and obesity. This review provides an overview of the role of SAPKs in the regulation of metabolism.
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