Τίτλος:
Cellular and molecular mediators of intestinal fibrosis
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Intestinal fibrosis is a major complication of the inflammatory bowel diseases (IBD) and although inflammation is necessary for its development, it would appear that it plays a minor role in its progression as anti-inflammatory treatments in IBD do not prevent fibrosis once it has started. The processes that regulate fibrosis would thus appear to be distinct from those regulating inflammation and, therefore, a detailed understanding of these pathways is vital to the development of antifibrogenic strategies. There have been several recent reviews exploring what is known, and what remains unknown, about the development of intestinal fibrosis. This review is designed to add to this literature but with a focus on the cellular components that are involved in the development of fibrogenesis and the major molecular mediators that impact on these cells. The aim is to heighten the understanding of the factors involved in intestinal fibrogenesis so that detailed research can be encouraged in order to advance the processes that could lead to effective treatments. © 2015 Published on behalf of European Crohn's and Colitis Organisation.
Συγγραφείς:
Lawrance, I.C.
Rogler, G.
Bamias, G.
Breynaert, C.
Florholmen, J.
Pellino, G.
Reif, S.
Speca, S.
Latella, G.
Περιοδικό:
Journal of Crohn's and Colitis
Εκδότης:
Oxford University Press
Λέξεις-κλειδιά:
activin; antifibrinolytic agent; chemokine; connective tissue growth factor; cytokine; epidermal growth factor; fibroblast growth factor; gamma interferon; platelet derived growth factor; reactive oxygen metabolite; somatomedin; transforming growth factor beta; tumor necrosis factor; cytokine; signal peptide, adaptive immunity; apoptosis; autophagy; cell proliferation; cell transformation; cytology; disease course; endothelium cell; epithelium cell; extracellular matrix; fibroblast; hematopoietic stem cell; human; immunocompetent cell; inflammatory bowel disease; innate immunity; intestinal fibrosis; mesenchyme cell; microvasculature; molecular pathology; myofibroblast; nonhuman; pericyte; priority journal; protein function; Review; risk assessment; risk factor; smooth muscle cell; stellate cell; stem cell; animal; complication; fibrosis; immune system; immunology; inflammatory bowel disease; intestine; metabolism; pathology; physiology, Animals; Apoptosis; Autophagy; Cell Proliferation; Cytokines; Fibroblasts; Fibrosis; Hematopoietic Stem Cells; Humans; Immune System; Inflammatory Bowel Diseases; Intercellular Signaling Peptides and Proteins; Intestines; Myocytes, Smooth Muscle; Myofibroblasts; Pericytes
DOI:
10.1016/j.crohns.2014.09.008
