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PI3K/AKT/PTEN pathway as a target for Crohn's disease therapy (Review)

Nana Tokuhira1, Yasuko Kitagishi1, Miho Suzuki1

  • 1Department of Food Science and Nutrition, Nara Women's University, Nara 630‑8506, Japan.

International Journal of Molecular Medicine
|October 30, 2014
PubMed

Insights

Loss-of-function mutations in NOD2 are linked to Crohn's disease, causing excessive gut inflammation. Understanding the PI3K/AKT/PTEN pathway

Area of Science:

  • Gastroenterology
  • Immunology
  • Molecular Biology

Background:

  • Inflammatory Bowel Disease (IBD), including Crohn's disease, pathogenesis is under intense investigation.
  • Nucleotide-binding oligomerization domain-containing protein 2 (NOD2) loss-of-function mutations are significant genetic risk factors for Crohn's disease.
  • This genetic predisposition results in exaggerated mucosal inflammation against gut microbiota.

Purpose of the Study:

  • To explore the role of reactive oxygen species (ROS) and the PI3K/AKT/PTEN pathway in Crohn's disease pathogenesis.
  • To identify potential molecular targets for novel therapeutic strategies against Crohn's disease.

Main Methods:

  • Review of existing literature on NOD2 mutations, ROS signaling, and the PI3K/AKT/PTEN pathway in IBD.
  • Analysis of the molecular mechanisms linking ROS, NF-κB activation, and inflammatory responses in Crohn's disease.

Main Results:

  • Reactive oxygen species (ROS) are implicated in inflammatory processes and cytokine signaling, including TNFα.
  • The PI3K/AKT/PTEN pathway, modulated by ROS via IKK, is crucial for NF-κB activation and plays a key role in Crohn's disease.
  • Loss of function in this pathway is an early event in various diseases, highlighting its significance.

Conclusions:

  • The PI3K/AKT/PTEN pathway is a critical component in the pathogenesis of Crohn's disease.
  • Understanding the molecular assemblies within this pathway offers potential for developing new therapeutic interventions for Crohn's disease.

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