Researchers at Helmholtz Munich, in collaboration with colleagues at Tohoku University, have identified a specific redox protein as a critical regulator of ferroptosis - a form of regulated oxidative cell death. Ferroptosis has garnered strong interest due to its therapeutic potential in addressing therapy-resistant and metastasizing cancers, and its involvement in neurodegenerative diseases. While sensitizing cancer cells to ferroptosis offers a promising anticancer approach, preventing neuronal ferroptosis may help slow the progression of neurodegenerative diseases such as Alzheimer's and multiple sclerosis (MS).
Consequently, research is focusing on novel cellular mechanisms that ultimately determine ferroptosis sensitivity. The team found that peroxiredoxin 6 (PRDX6) serves as a critical regulator of ferroptosis and acts as a selenium carrier protein, playing an essential role in cellular defense against oxidative stress. Their findings suggest that PRDX6 could become an important target for treating cancer and neurodegenerative diseases.
The study was published in Molecular Cell on November 14, 2024. The team was led by Dr. Eikan Mishima, Senior Scientist at the Institute of Metabolism and Cell Death at Helmholtz Munich and Tohoku University Graduate School of Medicine, and Professor Marcus Conrad from the Institute of Metabolism and Cell Death at Helmholtz Munich.
PRDX6: A selenium carrier protein and ferroptosis regulator Selenium, named after the Greek goddess of the .
