Researchers identify a signaling pathway that controls ADH5/GSNOR in SOD1 ALS cell models
Original source
Nuclear SOD1 links ATM-CHK2 signaling to ADH5/GSNOR transcription in SHSY-5Y SOD1G93A cellular models of ALS. (opens in a new tab)Compass summarised this from the study's abstract.
Study details
- Studied in
- Human
Related topics
Researchers identified a redox-dependent pathway involving ATM, CHK2 and SOD1 that increases production of ADH5/GSNOR in SH-SY5Y cells carrying the ALS-associated SOD1G93A mutation. Increasing ADH5/GSNOR protected these cells from SOD1G93A-related toxicity. The findings suggest a possible research strategy, but do not yet change treatment for people with ALS.
Why this matters
The work identifies molecular interactions that may help explain how cells respond to oxidative stress linked to mutant SOD1. It could guide further studies of ADH5/GSNOR, but the evidence comes from engineered cells rather than people or animals, so it has not demonstrated a clinical benefit.
Limitations and context
This was a laboratory study in SH-SY5Y cellular models expressing SOD1G93A, not a clinical trial or study in people. The proposed strategy has not been shown to improve disease outcomes or safety, and further work in relevant disease models and humans would be needed.