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Updated: Jul 6, 2025

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
Published on: March 15, 2024
Targeting ferroptosis and ferritinophagy: new targets for cardiovascular diseases
Yi Luan1, Yang Yang1, Ying Luan2
1Clinical Systems Biology Research Laboratories, Translational Medicine Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Insights
Iron-mediated cell death, ferroptosis, and its upstream mechanism, ferritinophagy, are critical in cardiovascular diseases (CVDs). Targeting these processes offers potential new therapeutic strategies for CVDs.
Area of Science:
- Biochemistry and Molecular Biology
- Cardiology
- Cell Biology
Background:
- Cardiovascular diseases (CVDs) are a primary global cause of mortality.
- The role of iron in CVDs is a long-standing area of research.
- Iron-mediated cell death, ferroptosis, and ferritinophagy are increasingly recognized in cardiac pathology.
Approach:
- This review delineates the mechanisms of ferroptosis and ferritinophagy.
- It explores regulatory pathways and molecular targets of ferritinophagy.
- The review examines the specific roles of these processes in CVDs.
Key Points:
- Ferritinophagy acts as an upstream inducer of ferroptosis.
- Both ferroptosis and ferritinophagy are implicated in cardiomyocyte damage and CVD progression.
- Understanding these iron-related cell death pathways is crucial for CVD research.
Conclusions:
- Targeting ferritinophagy-induced ferroptosis presents a promising therapeutic avenue for CVDs.
- This review provides insights into CVD pathology and potential therapeutic targets.
- Further research into modulating these pathways could lead to novel treatments.
Abstract:
Cardiovascular diseases (CVDs) are a leading factor driving mortality worldwide. Iron, an essential trace mineral, is important in numerous biological processes, and its role in CVDs has raised broad discussion for decades. Iron-mediated cell death, namely ferroptosis, has attracted much attention due to its critical role in cardiomyocyte damage and CVDs. Furthermore, ferritinophagy is the upstream mechanism that induces ferroptosis, and is closely related to CVDs. This review aims to delineate the processes and mechanisms of ferroptosis and ferritinophagy, and the regulatory pathways and molecular targets involved in ferritinophagy, and to determine their roles in CVDs. Furthermore, we discuss the possibility of targeting ferritinophagy-induced ferroptosis modulators for treating CVDs. Collectively, this review offers some new insights into the pathology of CVDs and identifies possible therapeutic targets.
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