向ATF6α减轻UVB诱导的衰老,并通过调节IL8表达来改善皮肤平衡
Joëlle Giroud1,2, Pauline Delvaux1, Laura Carlier1
1Laboratory of Biochemistry and Cell Biology (URBC), Namur Research Institute for Life Sciences (NARILIS), University of Namur, Namur, Belgium.
Aging cell
|April 17, 2025
概括
紫外线辐射通过诱导细胞衰老导致皮肤衰老. 研究人员发现,向ATF6α/IL8通路可能为皮肤衰老和相关疾病提供新的治疗方法.
科学领域:
- 皮肤病学 皮肤病学
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 皮肤衰老是由内在和外在因素造成的,特别是紫外线辐射,导致衰老细胞的积累.
- 紫外线暴露会触发皮肤细胞的衰老,如皮肤纤维细胞,但机制和表皮影响尚不清楚.
- 时间衰老和光衰老都会诱导人体皮肤中的未折叠蛋白质反应 (UPR).
研究的目的:
- 研究UV诱导皮肤细胞衰老的分子机制.
- 确定未折叠蛋白反应 (UPR) 和ATF6α在皮肤衰老中的作用.
- 探索ATF6α介导的衰老相关分泌表型 (SASP) 对表皮平衡的影响.
主要方法:
- 对老化和光衰老中的UPR标记物的人类皮肤样本的分析.
- 在暴露于UVB辐射的细胞中抑制ATF6α.
- 对衰老生物标志物和SASP成分的评估.
- 在重建的人类表皮中评估角质细胞的增殖.
主要成果:
- 时间老化和光衰老诱导人体皮肤细胞中的UPR.
- ATF6α沉默可以防止UVB诱导的衰老,并改变SASP.
- 改变的SASP会影响重建表皮中的角质细胞增殖.
- ATF6α部分调解IL8的表达,有助于角质细胞的过度增殖.
结论:
- 在皮肤光衰老过程中,ATF6α/IL8轴对调节邻近细胞平衡至关重要.
- ATF6α在紫外线引起的皮肤衰老中起着重要作用.
- 在皮肤衰老中,ATF6α 代表了 senotherapeutic 干预的潜在治疗点.
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