Molecular Mechanisms of Acute Radiation Intestinal Injury and Its Control

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  • Morita* Akinori
    Department of Biomedical Science and Technology, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japann
  • Nishiyama Yuichi
    Department of Biomedical Science and Technology, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japann
  • Sakai Takuma
    Department of Biomedical Science and Technology, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japann
  • Higashi Yuichi
    Department of Biomedical Science and Technology, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japann

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<p>The intestinal tract is a representative radiosensitive tissue and a risk organ in radiotherapy that limits the prescribed dose to tumors in the abdominal and pelvic regions. High-dose radiation damage to intestinal tissue induces the loss of intestinal epithelial stem cells, and it is now becoming clear that this process consists of two steps: crypt cell death regulated by p53 and exacerbation caused by inflammatory immune responses. Transcriptional regulators that enhance p53 function without enhancing apoptosis are effective in controlling the first step. The common activity of these p53 modulators that promote such functions is that they are able to suppress apoptosis without impairing p21-mediated cell cycle arrest. Regulating the second step can be achieved by agonists of Toll-like receptor signaling pathways that enhance the priming signal of pyroptosis and inhibitors that suppress the activity of the inflammasome. In this review, we outline the molecular mechanisms of each process and discuss strategies for effectively controlling the acute radiation-induced gastrointestinal syndrome.</p>

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