PM2.5 inhibits system Xc- activity to induce ferroptosis by activating the AMPK-Beclin1 pathway in acute lung injury

Yan, Kun; Hou, Tianhua; Zhu, Laiyu; Ci, Xinxin; Peng, Liping

doi:10.1016/j.ecoenv.2022.114083

Cited by 19 publications

(7 citation statements)

References 35 publications

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“…In addition, it has been reported that fine particulate matter in urban air can inhibit cell activity by activating the AMPK-Beclin1 pathway in ALI to induce ferroptosis. [31] Our study found that ALI is As a membrane-permeable free radical scavenger, Tempol can ameliorate LPS-induced ALI in mice through a mechanism in which superoxide anion plays a key role. [32] Tempol has multiple functions, such as protecting against various kidney-related diseases, including chronic ischemic kidney injury.…”

Section: Tempol Affects Gsh Synthesis Through Nrf2 Inhibits Ferroptos...mentioning

confidence: 56%

“…In addition, it has been reported that fine particulate matter in urban air can inhibit cell activity by activating the AMPK‐Beclin1 pathway in ALI to induce ferroptosis. [ 31 ] Our study found that ALI is associated with ferroptosis in lung epithelial cells. In vivo and in vitro, we explored the protective effects of Tempol against ALI and the potential mechanisms of Tempol use.…”

Section: Discussionmentioning

confidence: 67%

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Tempol alleviates acute lung injury by affecting glutathione synthesis through Nrf2 and inhibiting ferroptosis in lung epithelial cells

Ai,

Li,

Wang

et al. 2024

J Biochem & Molecular Tox

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As a life‐threatening disease, acute lung injury (ALI) may progress to chronic pulmonary fibrosis. For the treatment of lung injury, Tempol is a superoxide dismutase mimetic and intracellular redox agent that can be a potential drug. This study investigated the regulatory mechanism of Tempol in the treatment of ALI. A mouse model of ALI was established, and HE staining was used to examine histomorphology. The CCK‐8 assay was used to measure cell viability, and oxidative stress was assessed by corresponding kits. Flow cytometry and dichlorodihydrofluorescein diacetate staining assays were used to detect reactive oxygen species (ROS) levels. Protein expression levels were measured by Western blot analysis and ELISA. Pulmonary vascular permeability was used to measure the lung wet/dry weight ratio. The level of oxidative stress was increased in ALI mice, and the level of ferroptosis was upregulated. Tempol inhibited this effect and alleviated ALI. The administration of Tempol alleviated the pathological changes in ALI, inhibited pulmonary vascular permeability, and improved lung injury in ALI mice. The upregulation of genes essential for glutathione (GSH) metabolism induced by lipopolysaccharide (LPS) was inhibited by Tempol. In addition, nuclear factor‐related factor 2 (Nrf2) is activated by Tempol therapy to regulate the de novo synthesis pathway of GSH, thereby alleviating LPS‐induced lung epithelial cell damage. The results showed that Tempol alleviated ALI by activating the Nrf2 pathway to inhibit oxidative stress and ferroptosis in lung epithelial cells. In conclusion, this study demonstrates that Tempol alleviates ALI by inhibiting ferroptosis in lung epithelial cells through the effect of Nrf2 on GSH synthesis.

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Section: Tempol Affects Gsh Synthesis Through Nrf2 Inhibits Ferroptos...mentioning

confidence: 56%

Section: Discussionmentioning

confidence: 67%

Tempol alleviates acute lung injury by affecting glutathione synthesis through Nrf2 and inhibiting ferroptosis in lung epithelial cells

Ai,

Li,

Wang

et al. 2024

J Biochem & Molecular Tox

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“…Similarly, Yan et al. [ 42 ] observed that PM2.5 promotes ferroptosis by facilitating the BECN1-SLC7A11 complex in acute lung injury. In this context, the Co-IP results indicated an interaction between BECN1 and SLC7A11, which was bolstered by GRb1.…”

Section: Discussionmentioning

confidence: 90%

Ginsenoside Rb1 induces hepatic stellate cell ferroptosis to alleviate liver fibrosis via the BECN1/SLC7A11 axis

Lin,

Li,

et al. 2024

Journal of Pharmaceutical Analysis

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“…Moreover, AMPK can also promote ferroptosis by phosphorylating Beclin1 to inhibit the activity of system Xc − 96 . Beclin1 can bind to SLC7A11, the core component protein of system Xc − , resulting in downregulation of system Xc − transport capacity, reducing the source of raw materials required for glutathione synthesis, thereby inhibiting the antioxidant capacity of GPX4 and promoting the occurrence and development of ferroptosis 97 . Further studies showed that AMPK‐mediated phosphorylation of Beclin1 at Ser90, Ser93 and Ser96 sites is the key to the formation of Beclin1‐SLC7A11 complex.…”

Section: Potential Cross‐linking Pathways Between Autophagy and Ferro...mentioning

confidence: 99%

The association between ferroptosis and autophagy in cardiovascular diseases

Zhang,

Yang,

Ouyang

et al. 2024

Cell Biochemistry & Function

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Autophagy is a process in which cells degrade intracellular substances and play a variety of roles in cells, such as maintaining intracellular homeostasis, preventing cell overgrowth, and removing pathogens. It is highly conserved during the evolution of eukaryotic cells. So far, the study of autophagy is still a hot topic in the field of cytology. Ferroptosis is an iron‐dependent form of cell death, accompanied by the accumulation of reactive oxygen species and lipid peroxides. With the deepening of research, it has been found that ferroptosis, like autophagy, is involved in the occurrence and development of cardiovascular diseases. The relationship between autophagy and ferroptosis is complex, and the association between the two in cardiovascular disease remains to be clarified. This article reviews the mechanism of autophagy and ferroptosis and their correlation, and discusses the relationship between them in cardiovascular diseases, which is expected to provide new and important treatment strategies for cardiovascular diseases.

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PM2.5 inhibits system Xc- activity to induce ferroptosis by activating the AMPK-Beclin1 pathway in acute lung injury

Cited by 19 publications

References 35 publications

Tempol alleviates acute lung injury by affecting glutathione synthesis through Nrf2 and inhibiting ferroptosis in lung epithelial cells

Tempol alleviates acute lung injury by affecting glutathione synthesis through Nrf2 and inhibiting ferroptosis in lung epithelial cells

Ginsenoside Rb1 induces hepatic stellate cell ferroptosis to alleviate liver fibrosis via the BECN1/SLC7A11 axis

The association between ferroptosis and autophagy in cardiovascular diseases

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