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Deciphering ferroptosis in gene-edited mouse models
Yingying Yu1, Yizhou Lu1, Xuexian Fang2
1Department of Nutrition and Toxicology, School of Public Health and Nursing, Hangzhou Normal University, Hangzhou, China.
Abstract:
Ferroptosis, an iron-dependent form of regulated cell death, is increasingly recognized as a key mechanism in disease pathogenesis and treatment. As essential biomedical models, mice have played an instrumental role in uncovering the relationship between ferroptosis and disease. However, a systematic synthesis of phenotypic outcomes and mechanistic insights derived from these studies remains lacking. This review outlines the important molecular pathways of ferroptosis, including dysregulated iron metabolism, lipid peroxidation, and antiferroptotic defense systems, and highlights key genes involved in its regulation. We further integrate functional evidence from gene-edited mouse models to provide deeper insights into the pathophysiological relevance of ferroptosis across different disease contexts. Finally, promising yet underexplored areas are discussed to facilitate the clinical translation of ferroptosis research.
Insights
Ferroptosis, a cell death process, is vital in disease. This review synthesizes mouse model studies to clarify ferroptosis
Area of Science:
- Biomedical Science
- Cell Biology
- Pathophysiology
Background:
- Ferroptosis, an iron-dependent regulated cell death, is crucial in disease.
- Mice are key models for studying ferroptosis and disease links.
- A comprehensive review of ferroptosis research using mouse models is needed.
Purpose of the Study:
- To review ferroptosis molecular pathways and regulatory genes.
- To integrate evidence from gene-edited mouse models.
- To explore ferroptosis' pathophysiological relevance and clinical translation.
Main Methods:
- Literature review of ferroptosis mechanisms.
- Analysis of gene-edited mouse models.
- Synthesis of phenotypic and mechanistic insights.
Main Results:
- Detailed outline of ferroptosis pathways: iron metabolism, lipid peroxidation, and defense systems.
- Highlighting key regulatory genes in ferroptosis.
- Integration of functional data from mouse models demonstrating ferroptosis' role in diseases.
Conclusions:
- Ferroptosis is a significant factor in disease pathogenesis and treatment.
- Gene-edited mouse models offer valuable insights into ferroptosis.
- Further research can accelerate clinical applications of ferroptosis targeting.
