Matrix Metalloproteinases in Inflammatory Bowel Disease: An Update

Figure 1

Recently described signalling pathways in the gut leading to the upregulation of MMPs in IBD or models of colitis. The various mediators whose interaction with receptors on colonic epithelial cells, intestinal fibroblasts, myofibroblasts, and macrophages can trigger signal transduction pathways leading to increased expression of MMPs or TIMPs are shown. PI3Kγ (phosphatidylinositol-3 kinase γ), NF-κB (nuclear factor κB), TWEAK (TNF-related weak inducer of apoptosis), TGF-β (tissue growth factor β), cAMP (cyclic adenosine monophosphate), PKA (protein kinase A), VIP (vasoactive intestinal peptide), VPAC1 (vasoactive intestinal peptide receptor 1), MAPKs (mitogen activated protein kinases), ERK (extracellular signal-regulated kinase), PKC (protein kinase C), PKD (protein kinase D), and IL (interleukin).