4.3 Review

Possible Role of Toll-Like Receptor 4 in Acute Pancreatitis

Journal

PANCREAS
Volume 39, Issue 6, Pages 819-824

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MPA.0b013e3181ca065c

Keywords

acute pancreatitis; toll-like receptor 4

Funding

  1. Technological Foundation Project of Traditional Chinese Medicine Science of Zhejiang province [2003C130, 2004C142]
  2. Foundation Project for Medical Science and Technology of Zhejiang province [2003B134]
  3. Grave Foundation Project for Technological and Development of Hangzhou [2003123B19]
  4. Intensive Foundation Project for Technology of Hangzhou [2004Z006]
  5. Foundation Project for Medical Science and Technology of Hangzhou [2003A004]
  6. Foundation Project for Technology of Hangzhou [2005224]

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Because the mechanism underlying the development of acute pancreatitis (AP) has not yet been fully clarified, it has been a hot but difficult topic in basic and clinical research for a long time. Currently, the dominant hypothesis for the pathogenesis of AP is that it is a disease of self-digestive acute chemical inflammation induced by trypsin activation. As proteins to trigger the inflammatory response cascade, Toll-like receptors (TLRs), especially TLR4, provide a new clue for studying the pathogenesis of AP from the source. Some studies have found that when TLR4 is activated by certain factors, it can amplify an inflammatory effect and aggravate the body's inflammatory response through a series of signal transduction. Toll-like receptor 4 may play an important role in the synthesis and release of proinflammatory cytokines, and the up-regulation of the TLR4 gene may be related with the development and progression of multiple organ injury during AP. As the gate'' of inflammatory response, TLR4 may be closely associated with the development and progression of multiple organ injury during AP. Understanding the roles of TLR4 in AP will help to further clarify the pathogenesis of AP and to search a new target for the treatment of AP.

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