Helmholtz Zentrum München, German Research Centre for Environmental Health, Institute of Radiation Biology, Ingolstaedter Landstrasse 1, Neuherberg, 85764, Germany.
Adv Exp Med Biol. 2013;990:49-60. doi: 10.1007/978-94-007-5896-4_3.
Exposure of tumourous tissue to ionizing radiation initiates a wound-healing response involving remodelling of the extracellular microenvironment. The initial reaction involves direct damage to the matrix proteins and the secretion and activation of proteolytic enzymes that lead to local destruction of the extracellular matrix. Subsequently the wounded area may undergo complete repair, may enter a prolonged period of heightened proteolysis, or may overproduce matrix proteins leading to fibrosis. The source of matrix degrading enzymatic activity may be the tumour cells and the tumour stroma. Additional complexity is provided by proteolytic activity released from tissue macrophages, mast cells and by invading inflammatory cells. The local production of growth factors, including VEGF and TGF-β play a key role in coordinating the response. It is anticipated that the application of modern proteomic technologies will reveal hitherto unrecognised levels of complexity in these processes. Hopefully this will lead to the development of new therapeutic strategies to prevent long-term health implications of radiation exposure.
肿瘤组织暴露于电离辐射会引发伤口愈合反应，涉及细胞外微环境的重塑。最初的反应包括对基质蛋白的直接损伤，以及分泌和激活蛋白水解酶，导致细胞外基质的局部破坏。随后，受伤区域可能会完全修复，可能会进入一个延长的高蛋白酶解期，或者可能会过度产生基质蛋白导致纤维化。基质降解酶活性的来源可能是肿瘤细胞和肿瘤基质。组织巨噬细胞、肥大细胞和浸润的炎症细胞释放的蛋白水解活性增加了复杂性。包括 VEGF 和 TGF-β在内的生长因子的局部产生在协调反应中起着关键作用。预计现代蛋白质组学技术的应用将揭示这些过程中迄今尚未认识到的复杂性水平。希望这将导致开发新的治疗策略，以防止辐射暴露对长期健康的影响。
