Ferroptosis and mitochondrial dysfunction in acute central nervous system injury

Front. Cell. Neurosci., 2023 · DOI: 10.3389/fncel.2023.1228968 · Published: August 9, 2023

Simple Explanation

Acute central nervous system injuries (ACNSI), including traumatic brain injury (TBI) and stroke, lead to significant disability and death worldwide. Ferroptosis, a unique form of cell death involving lipid peroxidation and iron, plays a crucial role in neuropathological pathways linked to ACNSI. This review explores the connection between ferroptosis, mitochondrial dysfunction, and ACNSI to provide insights for researchers aiming to improve ACNSI treatment outcomes.

Study Duration

Not specified

Participants

Not specified

Evidence Level

Review

Key Findings

1
ACNSI can induce mitochondrial dysfunction, highlighting the importance of the mitochondrial connection to ferroptosis.
2
Anti-ferroptosis agents have shown potential in ameliorating the deleterious effects of ferroptosis in traumatic ACNSI.
3
Ferroptosis is closely associated with neurological functional deficits, neurodegenerative changes, neuroinflammatory responses, and blood-brain barrier damage following ACNSI.

Research Summary

Ferroptosis plays a significant role in ACNSI, particularly in secondary injury mechanisms, with mitochondrial dysfunction being a key contributor. Malfunctioning mitochondria can trigger oxidative stress, contributing to ferroptosis and neuronal cell death, suggesting that mitigating ferroptosis can reverse neural damage. Targeting mitochondria to counteract ferroptosis shows promise for treating ACNSI, but further research is needed to confirm effectiveness and safety.

Practical Implications

Targeted Therapies

Development of therapies specifically targeting mitochondria to prevent ferroptosis in ACNSI.

Drug Delivery Systems

Nanomaterials for precise drug delivery to mitochondria, optimizing drug release amount and location.

Mitochondrial Dynamics Regulation

Regulation of mitochondrial dynamics, including promoting splitting and merging of mitochondria and mitophagy, to counteract ferroptosis.

Study Limitations

1
Controversial mechanisms surrounding the role of mitochondria in ferroptosis.
2
Limited clinical experiments to confirm the effectiveness and safety of targeting mitochondria to counteract ferroptosis.
3
The implementation of ideas is currently limited to experimental settings

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