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Published on: March 15, 2024
Disulfidptosis: A new type of cell death
Abstract:
Disulfidptosis is a novel form of cell death that is distinguishable from established programmed cell death pathways such as apoptosis, pyroptosis, autophagy, ferroptosis, and oxeiptosis. This process is characterized by the rapid depletion of nicotinamide adenine dinucleotide phosphate (NADPH) in cells and high expression of solute carrier family 7 member 11 (SLC7A11) during glucose starvation, resulting in abnormal cystine accumulation, which subsequently induces andabnormal disulfide bond formation in actin cytoskeleton proteins, culminating in actin network collapse and disulfidptosis. This review aimed to summarize the underlying mechanisms, influencing factors, comparisons with traditional cell death pathways, associations with related diseases, application prospects, and future research directions related to disulfidptosis.
Insights
Disulfidptosis is a new cell death pathway. It involves NADPH depletion and cystine accumulation, causing disulfide bonds in actin and cell death, distinct from other programmed cell death types.
Area of Science:
- Cell Biology
- Biochemistry
- Pathology
Background:
- Discovered a novel cell death pathway termed disulfidptosis.
- Distinguishable from apoptosis, pyroptosis, autophagy, ferroptosis, and oxeiptosis.
- Characterized by rapid nicotinamide adenine dinucleotide phosphate (NADPH) depletion and solute carrier family 7 member 11 (SLC7A11) upregulation during glucose starvation.
Purpose of the Study:
- To review the mechanisms, influencing factors, and disease associations of disulfidptosis.
- To compare disulfidptosis with established programmed cell death pathways.
- To explore the application prospects and future research directions for disulfidptosis.
Main Methods:
- Literature review of disulfidptosis.
- Analysis of molecular mechanisms.
- Comparison with other cell death modalities.
Main Results:
- Disulfidptosis is triggered by glucose starvation, leading to NADPH depletion and SLC7A11 overexpression.
- Abnormal cystine accumulation results in aberrant disulfide bond formation in actin.
- Actin cytoskeleton collapse is the terminal event in disulfidptosis.
Conclusions:
- Disulfidptosis represents a distinct programmed cell death pathway.
- Understanding disulfidptosis mechanisms offers potential therapeutic targets for related diseases.
- Further research is needed to fully elucidate its role and applications.
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