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NFS1 Plays a Critical Role in Regulating Ferroptosis Homeostasis
Siying Sun1,2, Hanwen Cao1,2, Xuemei Li1,2,3,4,5
1School of Optometry, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Biomolecules
|January 28, 2026
Summary
Cysteine desulfurase (NFS1) regulates ferroptosis, a cell death pathway crucial in diseases. Its dysregulation impacts cancer, cardiovascular, and neurological conditions, highlighting NFS1 as a potential therapeutic target.
Area of Science:
- Biochemistry
- Cell Biology
- Pathology
Background:
- Ferroptosis is iron-dependent cell death linked to various diseases.
- NFS1 is vital for iron-sulfur cluster synthesis and ferroptosis regulation.
- NFS1's role in diseases like cancer and neurodegeneration is increasingly recognized.
Purpose of the Study:
- To review the molecular mechanisms of NFS1-mediated ferroptosis.
- To explore NFS1's role in diverse disease models.
- To identify NFS1 as a potential therapeutic target for ferroptosis-related diseases.
Main Methods:
- Systematic literature review of NFS1's function in ferroptosis.
- Analysis of NFS1's involvement in iron homeostasis and signaling pathways.
- Examination of NFS1 expression and its impact in disease contexts.
Main Results:
- NFS1 modulates ferroptosis via Fe-S cluster homeostasis and key signaling axes (ACO1/IRP1, Xc-/GSH-GPX4, p53/STAT).
- Altered NFS1 function leads to iron overload, ROS accumulation, and lipid peroxidation.
- NFS1 upregulation promotes tumor ferroptosis resistance, while downregulation impairs cardiomyocytes and neurons.
Conclusions:
- NFS1 is a critical regulator of cellular fate and ferroptosis.
- NFS1 presents significant therapeutic potential for cancer, neurological, and cardiovascular diseases.
- Further research into NFS1 mechanisms can guide targeted therapeutic strategies.
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