University of Namur, Research Unit on Cellular Biology, Rue de Bruxelles, 61, Namur B-5000, Belgium.
Adv Exp Med Biol. 2010;694:126-37. doi: 10.1007/978-1-4419-7002-2_10.
Oncogenic and environmental stresses, such as reactive oxygen species, UV radiation etc, can induce premature cellular senescence without critical telomere shortening. The role of the Ras/Raf/ERK signal transduction cascade in this process has been previously established, but recent evidence also indicates a critical role of the p38 MAP kinases pathway. Oncogenic and environmental stresses impinge upon the p38(MAPK) pathway, suggesting a major role of this pathway in senescence induced by stresses. Prematurely senescent cells are most likely to appear in several age-relatedpathologies associated with a stressful environment and/or the release of pro-inflammatory cytokines.
致癌和环境压力,如活性氧、紫外线辐射等,可在不发生关键端粒缩短的情况下诱导过早的细胞衰老。Ras/Raf/ERK 信号转导级联在这一过程中的作用以前已经确定,但最近的证据也表明 p38 MAP 激酶途径起着关键作用。致癌和环境压力作用于 p38(MAPK)途径,提示该途径在应激诱导的衰老中起着重要作用。与应激和/或促炎细胞因子释放相关的几种与年龄相关的病理中,很可能会出现过早衰老的细胞。