Discover how the innovative approach of neuron-targeted liposomal coenzyme Q10 offers a promising avenue for mitigating neuronal ferroptosis following subarachnoid hemorrhage, highlighting a breakthrough in neurosurgical oncology research.
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Neuron-targeted liposomal coenzyme Q10 attenuates neuronal ferroptosis after subarachnoid hemorrhage by activating the ferroptosis suppressor protein 1/coenzyme Q10 system.
Peng et al., Acta Biomater 2024
<!– DOI: 10.1016/j.actbio.2024.03.023 //–>
https://doi.org/10.1016/j.actbio.2024.03.023
Subarachnoid hemorrhage (SAH), often resulting from ruptured intracranial aneurysms, significantly disrupts the blood-brain barrier, leading to neuronal damage through ferroptosis—a form of cell death driven by iron accumulation and oxidative stress. A key player in combating this process is Ferroptosis Suppressor Protein 1 (FSP1), which protects neurons by converting Coenzyme Q10 (CoQ10) into a form that neutralizes reactive oxygen species. However, SAH depletes CoQ10, limiting FSP1’s protective role. Addressing this, researchers developed a neuron-targeted liposomal CoQ10, designed to deliver CoQ10 directly to neurons affected by SAH, thereby enhancing FSP1 function. This targeted approach not only increased FSP1 levels but also significantly reduced oxidative stress markers and neuronal ferroptosis in both cell cultures and animal models. This study introduces a novel therapeutic strategy that leverages targeted CoQ10 delivery to mitigate neuronal damage following SAH, offering a promising avenue for treating conditions associated with blood-brain barrier disruption and oxidative stress-induced neuronal injury.