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[Research News] Unveiling the Intricate Mechanisms Behind Oxysterol-Induced Cell Death
The research team, including Yasuomi URANO and Noriko NOGUCHI, professors at the F Graduate School of Life and Medical Sciences reveal that 25-hydroxycholesterol induces a particular type of cell death called ferroptosis, which could be implicated in several degenerative diseases.
Oxysterols, molecules derived from cholesterol, play crucial roles in our bodies but can also contribute to various diseases. Now, researchers from Japan have discovered that 25-hydroxycholesterol (25-OHC) triggers a specific type of cell death called ferroptosis in nerve-supporting cells. The study reveals that 25-OHC disrupts cellular protective mechanisms and antioxidant systems. These findings could lead to new diagnostics and treatments for conditions, like amyotrophic lateral sclerosis, where elevated 25-OHC levels have been observed.
Reference
Yasuomi Urano, Anan Iwagaki, Arisa Takeishi, Nazuna Uchiyama, Noriko Noguchi, Downregulation of the SREBP pathways and disruption of redox status by 25-hydroxycholesterol predispose cells to ferroptosis. Free Radical Biology and Medicine, Vol. 228, pp 319-328, 16 February 2025,
DOI:https://doi.org/10.1016/j.freeradbiomed.2025.01.010
For more details, please see the website of Organization for Research Initiatives and Development, Doshisha University.
https://research.doshisha.ac.jp/news/news-detail-69/
This achievement has also been featured in the “EurekAlert!.”
https://www.eurekalert.org/news-releases/1074198/

Image title: Overview of the proposed mechanism of 25-OHC-induced ferroptosis
Image caption: This image summarizes the main findings of the study, showing the multifaceted effects that exposure to 25-hydroxycholesterol (25-OHC) has on Schwann cells.
Image credit: Professor Yasuomi Urano from Doshisha University, Japan
License type: CC BY 4.0
Image source link:
https://www.sciencedirect.com/science/article/pii/S0891584925000103?via%3Dihub
Usage restrictions: You are free to share and adapt but credit must be given to the creator.
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