title: PI3K/AKT/PTEN pathway as a target for Crohn's disease therapy (Review).
abstract: The pathogenesis of inflammatory bowel disease (IBD), including Crohn's disease, is a subject of increasing interest. Loss-of-function mutations in nucleotide-binding oligomerization domain-containing protein 2 (NOD2) are strong genetic factors linked to Crohn's disease, which eventually leads to an excessive mucosal inflammatory response directed against components of normal gut microbiota. Reactive oxygen species (ROS) play an important role in inflammation processes, as well as in transduction of signals from receptors for several cytokines, such as tumor necrosis factor α (TNFα). ROS activate nuclear factor-κB (NF-κB) via IκB kinase (IKK) through the PI3K/AKT/PTEN pathway. Therefore, this pathway is recognized to play a key role in Crohn's disease. Loss of function has been demonstrated to occur as an early event in a wide variety of diseases. Given this prevalent involvement in a number of diseases, the molecular development that modulates this pathway has been the subject of several studies. In addition, it has been the focus of extensive research and drug discovery activities. A better understanding of the molecular assemblies may reveal novel targets for the therapeutic development against Crohn's disease.
authors.affiliation: Department of Food Science and Nutrition, Nara Women's University, Nara 630‑8506, Japan.
authors.forename: Nana
authors.initials: N
authors.lastname: Tokuhira
authors.affiliation: Department of Food Science and Nutrition, Nara Women's University, Nara 630‑8506, Japan.
authors.forename: Yasuko
authors.initials: Y
authors.lastname: Kitagishi
authors.affiliation: Department of Food Science and Nutrition, Nara Women's University, Nara 630‑8506, Japan.
authors.forename: Miho
authors.initials: M
authors.lastname: Suzuki
authors.affiliation: Department of Food Science and Nutrition, Nara Women's University, Nara 630‑8506, Japan.
authors.forename: Akari
authors.initials: A
authors.lastname: Minami
authors.affiliation: Department of Food Science and Nutrition, Nara Women's University, Nara 630‑8506, Japan.
authors.forename: Atsuko
authors.initials: A
authors.lastname: Nakanishi
authors.affiliation: Department of Food Science and Nutrition, Nara Women's University, Nara 630‑8506, Japan.
authors.forename: Yuna
authors.initials: Y
authors.lastname: Ono
authors.affiliation: Department of Food Science and Nutrition, Nara Women's University, Nara 630‑8506, Japan.
authors.forename: Keiko
authors.initials: K
authors.lastname: Kobayashi
authors.affiliation: Department of Food Science and Nutrition, Nara Women's University, Nara 630‑8506, Japan.
authors.forename: Satoru
authors.initials: S
authors.lastname: Matsuda
authors.affiliation: Department of Food Science and Nutrition, Nara Women's University, Nara 630‑8506, Japan.
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Ogura
mesh_terms: D000818:Animals; D003424:Crohn Disease / Q000188:drug therapy* / Q000378:metabolism*; D004032:Diet; D004791:Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D058990:Molecular Targeted Therapy; D053473:Nod2 Signaling Adaptor Protein / Q000378:metabolism; D051059:PTEN Phosphohydrolase / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism
chemical_list: D004791:Enzyme Inhibitors; D053473:Nod2 Signaling Adaptor Protein; D051059:PTEN Phosphohydrolase; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases