Publications by authors named "Yi-Yue Jiang"
KA-mediated excitotoxicity induces neuronal ferroptosis through activation of ferritinophagy.
CNS Neurosci Ther
September 2024
Objectives: This study aims to elucidate the role of Fe overload in kainic acid (KA)-induced excitotoxicity, investigate the involvement of ferritinophagy selective cargo receptor NCOA4 in the pathogenesis of excitotoxicity.
Methods: Western blotting was used to detect the expression of FTH1, NCOA4, Lamp2, TfR, FPN, and DMT1 after KA stereotaxic injection into the unilateral striatum of mice. Colocalization of Fe with lysosomes in KA-treated primary cortical neurons was observed by using confocal microscopy.
Article Synopsis
- Excitotoxicity is a key factor in neurodegenerative diseases, and its connection to ferroptosis (a form of cell death) is not well understood.
- This study finds that NADPH not only acts as a reductant but also interacts with N-myristoyltransferase 2 (NMT2), leading to increased levels of a protein (FSP1) that helps resist ferroptosis.
- The research highlights that the interaction between NADPH, NMT2, and FSP1 is crucial for understanding how neurons can withstand ferroptosis, potentially offering new avenues for treating related diseases.
Article Synopsis
- Excitotoxicity occurs when excessive levels of excitatory amino acids lead to neuron damage, playing a critical role in neurodegenerative diseases.
- The protein TP53 is linked to excitotoxicity, and its pathway involving the TIGAR regulator can help protect neurons from injury.
- In a mouse model, kainic acid (KA) was shown to decrease TIGAR levels and worsen neuroinflammation and mitochondrial issues; however, overexpressing TIGAR helped reverse these effects, suggesting it as a potential treatment target for neurodegenerative diseases.