Zemljic Mateja, Pejkovic Bozena, Krajnc Ivan, Lipovsek Saska
Institute of Anatomy, Histology and Embryology, Faculty of Medicine, University of Maribor, Ljubljanska 5, 2000, Maribor, Slovenia,
Wien Klin Wochenschr. 2014 Oct;126(19-20):626-33. doi: 10.1007/s00508-014-0592-7. Epub 2014 Sep 26.
Apoptosis, 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.
细胞凋亡、自噬和坏死是哺乳动物细胞死亡网络的三种不同功能类型。它们都具有一些细胞形态学变化的特征。细胞死亡的不适当诱导与多种疾病的发病机制有关。炎症性肠病（溃疡性结肠炎、克罗恩病）的发病机制包括对肠道微生物群紊乱的异常免疫反应。慢性炎症性疾病及随后多器官病变发病机制中最重要的原因之一是肠道的屏障功能，它调节细胞活力。最近的研究结果已开始解释肠道上皮细胞在这种环境中得以存活的机制，以及正常调节过程的丧失如何导致炎症性肠病（IBD）。本综述聚焦于IBD发育和内环境稳态中生物学途径的调节。更好地理解生物学途径的生理功能及其对炎症、免疫和屏障功能的影响，将简化我们对胃肠道内环境稳态的认识，并改善诊断和治疗。
