Lipid peroxidation in neurodegeneration

Peña-Bautista, Carmen; Vento, Máximo; Baquero, Miguel; Cháfer-Pericás, Consuelo

doi:10.1016/j.cca.2019.07.037

Cited by 68 publications

(43 citation statements)

References 136 publications

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“…Ferroptosis is kind of iron-dependent programmed cell death, regulated by lipid oxidation. This cell death is implicated in many disease pathologies, such as neurodegeneration, inflammation, and ischemia-reperfusion injury [24,[39][40][41]. In this study, we mainly explored the position of ferroptosis in LPS-induced ALI.…”

Section: Discussionmentioning

confidence: 99%

Ferrostatin-1 alleviates lipopolysaccharide-induced acute lung injury via inhibiting ferroptosis

et al. 2020

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Background: Ferroptosis is a newly recognized type of cell death, which is different from traditional necrosis, apoptosis or autophagic cell death. However, the position of ferroptosis in lipopolysaccharide (LPS)-induced acute lung injury (ALI) has not been explored intensively so far. In this study, we mainly analyzed the relationship between ferroptosis and LPS-induced ALI. Methods: In this study, a human bronchial epithelial cell line, BEAS-2B, was treated with LPS and ferrostatin-1 (Fer-1, ferroptosis inhibitor). The cell viability was measured using CCK-8. Additionally, the levels of malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), and iron, as well as the protein level of SLC7A11 and GPX4, were measured in different groups. To further confirm the in vitro results, an ALI model was induced by LPS in mice, and the therapeutic action of Fer-1 and ferroptosis level in lung tissues were evaluated. Results: The cell viability of BEAS-2B was down-regulated by LPS treatment, together with the ferroptosis markers SLC7A11 and GPX4, while the levels of MDA, 4-HNE and total iron were increased by LPS treatment in a dose-dependent manner, which could be rescued by Fer-1. The results of the in vivo experiment also indicated that Fer-1 exerted therapeutic action against LPS-induced ALI, and down-regulated the ferroptosis level in lung tissues. Conclusions: Our study indicated that ferroptosis has an important role in the progression of LPS-induced ALI, and ferroptosis may become a novel target in the treatment of ALI patients.

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Section: Discussionmentioning

confidence: 99%

Ferrostatin-1 alleviates lipopolysaccharide-induced acute lung injury via inhibiting ferroptosis

et al. 2020

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“…Mounting evidence suggests that ferroptosis is the major cell death modality associated with ischemic organ injuries, including ischemic heart disease and kidney failure (Friedmann Angeli et al, 2014;Gao et al, 2015;Linkermann et al, 2014). Ferroptosis has also been implicated as a pathological contributor to neurodegenerative diseases (DeGregorio-Rocasolano et al, 2019;Pena-Bautista et al, 2019). In addition, the death of oligodendrocytes in models of Pelizaeus-Merzbacher disease is due to ferroptosis (Nobuta et al, 2019).…”

Section: Other Diseasesmentioning

confidence: 99%

The Chemistry and Biology of Ferroptosis

Stockwell

Jiang

2020

Cell Chemical Biology

248

203

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Àinhibitor (Gout et al., 2001). However, sulfasalazine has very low potency, and is metabolically unstable in vivo, making it difficult to use in animal studies; it is best used as a confirmatory tool in cell culture studies. The compounds DPI2 (Yang et al., 2014) and RSL5 (Yang and Stockwell, 2008) have similar effects as erastin, and may also be system x c À inhibitors, although this potential mechanism has not been tested directly (Figure 1; Table 1).The amino acid and neurotransmitter glutamate has also been shown to inhibit system x c À and to induce ferroptosis in some cellular contexts (Murphy et al., 1989). Glutamate has a variety

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“…Mitochondrial lipid peroxidation may be a key process in the development of ferroptosis in neurodegenerative diseases [154]. In an early study of the connection between GPX4 knockout and neurodegeneration, it was found that inhibition of the GSH/GPx4 system converts oxidative stress into a 12/15-LOX-dependent lipid peroxide signal that finally activates apoptosis-inducing factor (AIF) [9].…”

Section: Relationship Between Ferroptosis and Mitochondria In Neurodementioning

confidence: 99%

Ferroptosis Is Regulated by Mitochondria in Neurodegenerative Diseases

et al. 2020

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Background: Neurodegenerative diseases are characterized by a gradual decline in motor and/or cognitive function caused by the selective degeneration and loss of neurons in the central nervous system, but their pathological mechanism is still unclear. Previous research has revealed that many forms of cell death, such as apoptosis and necrosis, occur in neurodegenerative diseases. Research in recent years has noticed that there is a new type of cell death in neurodegenerative diseases: ferroptosis. An increasing body of literature provides evidence for an involvement of ferroptosis in neurodegenerative diseases. Summary: In this article, we review a new form of cell death in neurodegenerative diseases: ferroptosis. Ferroptosis is defined as an iron-dependent form of regulated cell death, which occurs through the lethal accumulation of lipid-based reactive oxygen species when glutathione-dependent lipid peroxide repair systems are compromised. Several salient and established features of neurodegenerative diseases (including lipid peroxidation and iron dyshomeostasis) are consistent with ferroptosis, which means that ferroptosis may be involved in the progression of neurodegenerative diseases. In addition, as the center of energy metabolism in cells, mitochondria are also closely related to the regulation of iron homeostasis in the nervous system. At the same time, neurodegenerative diseases are often accompanied by degeneration of mitochondrial activity. Mitochondrial damage has been found to be involved in lipid peroxidation and iron dyshomeostasis in neurodegenerative diseases. Key Messages: Based on the summary of the related mechanisms of ferroptosis, we conclude that mitochondrial damage may affect neurodegenerative diseases by regulating many aspects of ferroptosis, including cell metabolism, iron dyshomeostasis, and lipid peroxidation.

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Lipid peroxidation in neurodegeneration

Cited by 68 publications

References 136 publications

Ferrostatin-1 alleviates lipopolysaccharide-induced acute lung injury via inhibiting ferroptosis

Ferrostatin-1 alleviates lipopolysaccharide-induced acute lung injury via inhibiting ferroptosis

The Chemistry and Biology of Ferroptosis

Ferroptosis Is Regulated by Mitochondria in Neurodegenerative Diseases

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