Mitochondrial ferritin upregulation by deferiprone reduced neuronal ferroptosis and improved neurological deficits via NDRG1/Yap pathway in a neonatal rat model of germinal matrix hemorrhage.

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Tác giả: Xionghui Chen, Siyuan Dong, Jerry J Flores, Lingui Gu, Mingyang Han, Qiuguang He, Lei Huang, Hideki Kanamaru, Ruihao Li, Jiping Tang, Yihao Tao, Lei Wu, Zongyi Xie, Xiao Yang, Kun Yi, Ye Yuan, John H Zhang, Xingyu Zhang, Yutong Zhao, Shiyi Zhu

Ngôn ngữ: eng

Ký hiệu phân loại: 912.01 Philosophy and theory

Thông tin xuất bản: United States : Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 251331

Ferroptosis contributes to brain injury after germinal matrix hemorrhage (GMH). Mitochondrial ferritin (FTMT), a novel mitochondrial outer membrane protein, reduces oxidative stress in neurodegenerative diseases. In vitro, Deferiprone has been shown to upregulate FTMT. However, the effects of FTMT upregulation by Deferiprone on neuronal ferroptosis after GMH and its underlying mechanism has not been investigated. In our study, 389 Sprague-Dawley rat pups of postnatal day 7 were used to establish a collagenase-induced GMH model and an iron-overload model of intracerebral FeCl
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