期刊
MOLECULAR MEDICINE
卷 20, 期 -, 页码 466-477出版社
SPRINGER
DOI: 10.2119/molmed.2014.00117
关键词
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资金
- National Institutes of Health [R01CA160417, R01CA181450]
- Pancreatic Cancer Action Network-AACR Career Development Award [13-20-25-TANG]
- University of Pittsburgh Cancer Institute [P30CA047904]
Cell death and inflammation are key pathologic responses of acute pancreatitis (AP), the leading cause of hospital admissions for gastrointestinal disorders. It is becoming increasingly clear that damage-associated molecular pattern molecules (DAMPs) play an important role in the pathogenesis of AP by linking local tissue damage to systemic inflammation syndrome. Endogenous DAMPs released from dead, dying or injured cells initiate and extend sterile inflammation via specific pattern recognition receptors. Inhibition of the release and activity of DAMPs (for example, high mobility group box 1, DNA, histones and adenosine triphosphate) provides significant protection against experimental AP. Moreover, increased serum levels of DAMPs in patients with AP correlate with disease severity. These findings provide novel insight into the mechanism, diagnosis and management of AP. DAMPs might be an attractive therapeutic target in AP.
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