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. Author manuscript; available in PMC: 2016 Aug 25.
Published in final edited form as: Radiat Res. 2016 Jul 7;186(2):153–161. doi: 10.1667/RR14445.1

FIG. 1.

FIG. 1

Ionizing radiation induces endothelial cell apoptosis and senescence in a dose-dependent manner. Exposure of endothelial cells to a very high dose (>10 Gy) of ionizing radiation (IR) induces apoptosis via activation of the acidic sphingomyelinase (aSMase) that hydrolyzes sphingomyelin (SM) on the plasma membrane to generate ceramide and to induce Bax and Bak. However, exposure of endothelial cells to a moderate (>0.5 Gy) or high dose (<10 Gy) of radiation primarily induces senescence via multiple pathways, as shown. ALK5, TGF-β type 1 receptor kinase; ATM, ataxia-telangiectasia mutated protein kinase; CHK2, checkpoint kinase 2; DSBs, DNA double-strand breaks; IGF1R, insulin-like factor-1 receptor; mTOR, mechanistic target of rapamycin; NFκB, nuclear factor κB; p38, p38 mitogen-activated protein kinases; PI3K, phosphtidylinositol-3-kinase; ROS, reactive oxygen species; and TGF-β, tumor growth factor β.