• Mateja Zemljic, Bozena Pejkovic, Ivan Krajnc, and Saska Lipovsek.
• Institute of Anatomy, Histology and Embryology, Faculty of Medicine, University of Maribor, Ljubljanska 5, 2000, Maribor, Slovenia, mateja.zemljic@gmail.com.
• Wien. Klin. Wochenschr. 2014 Oct 1; 126 (19-20): 626-33.

AbstractApoptosis, autophagy and necrosis are three distinct functional types of the mammalian cell death network. All of them are characterized by a number of cell's morphological changes. The inappropriate induction of cell death is involved in the pathogenesis of a number of diseases.Pathogenesis of inflammatory bowel diseases (ulcerative colitis, Crohn's disease) includes an abnormal immunological response to disturbed intestinal microflora. One of the most important reason in pathogenesis of chronic inflammatory disease and subsequent multiple organ pathology is a barrier function of the gut, regulating cellular viability. Recent findings have begun to explain the mechanisms by which intestinal epithelial cells are able to survive in such an environment and how loss of normal regulatory processes may lead to inflammatory bowel disease (IBD).This review focuses on the regulation of biological pathways in development and homeostasis in IBD. Better understanding of the physiological functions of biological pathways and their influence on inflammation, immunity, and barrier function will simplify our expertice of homeostasis in the gastrointestinal tract and in upgrading diagnosis and treatment.

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