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From Extracellular to Intracellular Targets, Inhibiting MAP Kinases in Treatment of Crohn's Disease
Author(s) -
BLINK BERNT,
HOVE TESSA,
BRINK GIJS R.,
PEPPELENBOSCH MAIKEL P.,
DEVENTER SANDER J.H.
Publication year - 2002
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2002.tb04664.x
Subject(s) - mapk/erk pathway , crohn's disease , intracellular , inflammation , signal transduction , immunology , extracellular , disease , mediator , medicine , kinase , inflammatory bowel disease , biology , cancer research , bioinformatics , microbiology and biotechnology
A bstract : In recent years the emphasis in finding new therapeutic options for chronic inflammatory diseases has been on targeting extracellular mediators of inflammation. A range of tools has become available to interfere with signaling by cytokines and their receptors. As our understanding of the intracellular pathways that mediate inflammatory signals expands, new therapeutic targets within the inflammatory cells come into sight. In this review we will discuss possible intracellular targets for treatment in Crohn's disease, a chronic relapsing inflammatory disease of the gut. Despite the encouraging results with anti‐TNF antibodies in patients with Crohn's disease, our current treatment options are still insufficient and warrant novel treatment strategies. The mitogen‐activated protein kinase (MAPK) family of signal transduction proteins is an important intracellular mediator of inflammation, and recently a MAPK inhibitor was successfully used in patients with Crohn's disease. We will discuss our current understanding of the molecular pathophysiology of Crohn's disease and also novel therapies that specifically target members of the MAPK pathway.