Molecular and Computational Biology Program, Department of Biological Sciences, Dornsife College of Letters, Arts, and Sciences, University of Southern California, Los Angeles, CA, USA; Leonard Davis School of Gerontology, Ethel Percy Andrus Gerontology Center, University of Southern California, Los Angeles, CA90089, USA.
National Institute on General Medical Sciences, National Institutes of Health, Bethesda, MD, 20892, USA.
Redox Biol. 2020 Apr;31:101488. doi: 10.1016/j.redox.2020.101488. Epub 2020 Mar 9.
Sex differences in diseases involving oxidative and proteolytic stress are common, including greater ischemic heart disease, Parkinson disease and stroke in men, and greater Alzheimer disease in women. Sex differences are also observed in stress response of cells and tissues, where female cells are generally more resistant to heat and oxidative stress-induced cell death. Studies implicate beneficial effects of estrogen, as well as cell-autonomous effects including superior mitochondrial function and increased expression of stress response genes in female cells relative to male cells. The p53 and forkhead box (FOX)-family genes, heat shock proteins (HSPs), and the apoptosis and autophagy pathways appear particularly important in mediating sex differences in stress response.
涉及氧化应激和蛋白水解应激的疾病中存在性别差异是很常见的，包括男性中更常见的缺血性心脏病、帕金森病和中风，以及女性中更常见的阿尔茨海默病。在细胞和组织的应激反应中也观察到性别差异，女性细胞通常对热和氧化应激诱导的细胞死亡有更强的抵抗力。研究表明，雌激素以及细胞自主效应，包括女性细胞中线粒体功能的改善和应激反应基因的表达增加，都与这些性别差异有关。p53 和叉头框（FOX）家族基因、热休克蛋白（HSPs）以及凋亡和自噬途径在介导应激反应中的性别差异方面似乎尤为重要。
