Blue light induces skin apoptosis and degeneration through activation of the endoplasmic reticulum stress-autophagy apoptosis axis: Protective role of hydrogen sulfide

自噬 未折叠蛋白反应 内质网 细胞生物学 细胞凋亡 程序性细胞死亡 氧化应激 活性氧 化学 生物 生物化学
作者
Sen Zhu,Xuan Li,Fen Wu,Xinhui Cao,Kexin Gou,Chunming Wang,Changjun Lin
出处
期刊:Journal of Photochemistry and Photobiology B-biology [Elsevier]
卷期号:229: 112426-112426 被引量:9
标识
DOI:10.1016/j.jphotobiol.2022.112426
摘要

Research on the phototoxicity of blue light (BL) to the skin is increasing. Although blue light can induce oxidative stress, inflammation, and inhibition of proliferation in skin cells, the mechanism by which blue light damages the skin is not yet clear. Endoplasmic reticulum (ER) stress and autophagy are two mechanisms by which cells resist external interference factors and maintain cell homeostasis and normal function, and both can affect cell apoptosis. Interestingly, we have found that blue light (435 nm ~ 445 nm, 8000 lx, 6-24 h)-induced oxidative stress triggers the ER stress-CHOP (C/EBP homologous protein) signal and affects the protein levels of B-cell lymphoma-2 (Bcl-2) and Bcl2-associated X (Bax), thereby promoting apoptosis. In addition, blue light activates autophagy in skin cells, which intensifies cell death. When ER stress is inhibited, autophagy is subsequently inhibited, suggesting that blue light-induced autophagy is influenced by ER stress. These evidences suggest that blue light induces activation of reactive oxygen species (ROS)-ER stress-autophagy-apoptosis axis signaling, which further induces skin injury and apoptosis. This is the first report on the relationships among oxidative stress, ER stress, autophagy, and apoptosis in blue light-induced skin injury. Furthermore, we have studied the effect of hydrogen sulfide (H2S) on blue light-induced skin damage, and found that exogenous H2S can protect skin from blue light-induced damage by regulating the ROS-ER stress-autophagy-apoptosis axis. Our data shows that when we are exposed to blue light, such as sunbathing and jaundice treatment, H2S may be developed as a protective agent.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
思源应助咪咪不吃糖采纳,获得10
1秒前
2秒前
科研通AI2S应助葛子康采纳,获得10
2秒前
3秒前
青柠完成签到,获得积分10
3秒前
香蕉觅云应助jjl采纳,获得10
4秒前
毛豆应助valar采纳,获得10
4秒前
香蕉觅云应助活泼的不可采纳,获得10
4秒前
星河完成签到,获得积分10
5秒前
在水一方应助科研通管家采纳,获得10
5秒前
SciGPT应助科研通管家采纳,获得10
5秒前
Akim应助科研通管家采纳,获得10
5秒前
Lucas应助科研通管家采纳,获得10
5秒前
共享精神应助科研通管家采纳,获得10
5秒前
星辰大海应助科研通管家采纳,获得10
5秒前
Lucas应助科研通管家采纳,获得30
5秒前
共享精神应助科研通管家采纳,获得10
5秒前
无花果应助科研通管家采纳,获得10
5秒前
彭于晏应助科研通管家采纳,获得10
5秒前
NexusExplorer应助科研通管家采纳,获得10
5秒前
华仔应助科研通管家采纳,获得10
5秒前
情怀应助科研通管家采纳,获得10
5秒前
领导范儿应助科研通管家采纳,获得10
5秒前
天天快乐应助科研通管家采纳,获得10
5秒前
英姑应助科研通管家采纳,获得10
6秒前
6秒前
6秒前
Ksharp10发布了新的文献求助10
7秒前
RT发布了新的文献求助10
7秒前
小蘑菇应助yokkio采纳,获得10
7秒前
8秒前
Crystal发布了新的文献求助10
9秒前
9秒前
9秒前
9秒前
9秒前
10秒前
狗蛋儿真棒棒完成签到,获得积分10
11秒前
Granger完成签到 ,获得积分10
11秒前
isfj发布了新的文献求助10
11秒前
高分求助中
Spray / Wall-interaction Modelling by Dimensionless Data Analysis 2000
ALA生合成不全マウスでの糖代謝異常の分子機構解析 520
安全防范技术与工程 500
Mathematics and Finite Element Discretizations of Incompressible Navier—Stokes Flows 500
2-Acetyl-1-pyrroline: an important aroma component of cooked rice 500
A real-time energy management strategy based on fuzzy control and ECMS for PHEVs 400
2024 Medicinal Chemistry Reviews 400
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3191125
求助须知:如何正确求助?哪些是违规求助? 2840488
关于积分的说明 8028591
捐赠科研通 2503810
什么是DOI,文献DOI怎么找? 1337205
科研通“疑难数据库(出版商)”最低求助积分说明 638034
邀请新用户注册赠送积分活动 606497