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Hypoxia and ferroptosis.
Liu, Xiao-Qian; Shi, Meng-Zhen; Bai, Yu-Ting; Su, Xiao-Ling; Liu, Yan-Min; Wu, Jin-Chun; Chen, Li-Rong.
Afiliación
  • Liu XQ; Qinghai University, Xining 810001, PR China; Qinghai Provincial People's Hospital, Xining 810001, PR China.
  • Shi MZ; Qinghai University, Xining 810001, PR China; Qinghai Provincial People's Hospital, Xining 810001, PR China.
  • Bai YT; Qinghai Provincial People's Hospital, Xining 810001, PR China. Electronic address: baiyuting1226@163.com.
  • Su XL; Qinghai Provincial People's Hospital, Xining 810001, PR China.
  • Liu YM; Qinghai Provincial People's Hospital, Xining 810001, PR China.
  • Wu JC; Qinghai Provincial People's Hospital, Xining 810001, PR China.
  • Chen LR; Qinghai University, Xining 810001, PR China; Qinghai Provincial People's Hospital, Xining 810001, PR China.
Cell Signal ; 122: 111328, 2024 Jul 31.
Article en En | MEDLINE | ID: mdl-39094672
ABSTRACT
Ferroptosis is a novel, iron-dependent cell death characterized by the excessive accumulation of ferroptosis lipid peroxides ultimately leading to oxidative damage to the cell membrane. Iron, lipid, amino acid metabolism, and other signaling pathways all control ferroptosis. Numerous bodily tissues experience hypoxia under normal and pathological circumstances. Tissue cells can adjust to these changes by activating the hypoxia-inducible factor (HIF) signaling pathway and other mechanisms in response to the hypoxic environment. In recent years, there has been increasing evidence that hypoxia and ferroptosis are closely linked, and that hypoxia can regulate ferroptosis in specific cells and conditions through different pathways. In this paper, we review the possible positive and negative regulatory mechanisms of ferroptosis by hypoxia-inducible factors, as well as ferroptosis-associated ischemic diseases, with the intention of delivering novel therapeutic avenues for the defense and management of hypoxic illnesses linked to ferroptosis.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Idioma: En Revista: Cell Signal Año: 2024 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Idioma: En Revista: Cell Signal Año: 2024 Tipo del documento: Article