Damage to normal tissue is a limiting factor for clinical radiation for cancer eradication. Ionizing radiation can induce a variety of cellular responses, including apoptosis, necrosis, necroptosis, autophagy, and accelerated senescence.1 The molecular mechanisms of radiation-induced cellular injury depend on a number of factors, including radiation dosage and dose rate, cell type, transformed status, and growth rate. Recent studies suggest that accelerated senescence is a primary response of normal, untrans-formed epithelial and endothelial cells to radiation exposure.
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