p53 Controls Radiation-Induced Gastrointestinal Syndrome in Mice Independent of Apoptosis

Abstract

Gut Check The gastrointestinal (GI) tract is particularly sensitive to damage by ionizing radiation. Despite decades of study, fundamental questions such as which cells and which molecular mechanisms mediate this GI damage remain a source of great controversy. Studying a series of genetically manipulated mice, Kirsch et al. (p. 593 , published online 17 December) conclude that GI epithelial cells, rather than endothelial cells, are the critical cellular targets of radiation damage and that apoptosis (a well-studied mechanism of cell death) is not a major contributor to the damage. Rather, an alternative cell-death pathway whose activity is inhibited by the tumor suppressor protein p53 appears to mediate GI damage. Further insights into this pathway may assist the development of medical counter-measures for preventing and treating radiation-induced tissue damage.