Nature Communications (Feb 2019)
Macrophage achieves self-protection against oxidative stress-induced ageing through the Mst-Nrf2 axis
- Ping Wang,
- Jing Geng,
- Jiahui Gao,
- Hao Zhao,
- Junhong Li,
- Yiran Shi,
- Bingying Yang,
- Chen Xiao,
- Yueyue Linghu,
- Xiufeng Sun,
- Xin Chen,
- Lixin Hong,
- Funiu Qin,
- Xun Li,
- Jau-Song Yu,
- Han You,
- Zengqiang Yuan,
- Dawang Zhou,
- Randy L. Johnson,
- Lanfen Chen
Affiliations
- Ping Wang
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Jing Geng
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Jiahui Gao
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Hao Zhao
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Junhong Li
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Yiran Shi
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Bingying Yang
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Chen Xiao
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Yueyue Linghu
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Xiufeng Sun
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Xin Chen
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Lixin Hong
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Funiu Qin
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Xun Li
- Medical College of Xiamen University
- Jau-Song Yu
- Molecular Medicine Research Center, Chang Gung University and Liver Research Center, Chang Gung Memorial Hospital at Linkou
- Han You
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Zengqiang Yuan
- The Brain Science Center, Beijing Institute of Basic Medical Sciences
- Dawang Zhou
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- Randy L. Johnson
- Department of Biochemistry and Molecular Biology, University of Texas, M.D. Anderson Cancer Center
- Lanfen Chen
- State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University
- DOI
- https://doi.org/10.1038/s41467-019-08680-6
- Journal volume & issue
-
Vol. 10,
no. 1
pp. 1 – 16
Abstract
Immune cells produce reactive oxygen species (ROS) to eliminate pathogens, but cell-spontaneous death and ageing may also be induced. Here the authors show that, upon sensing ROS, Mst1/2 kinases modulate the activity of Nrf2 transcription factor and downstream genetic programs to protect mouse macrophages from death and ageing.