Ferroptosis is Involved in Hyperoxic Lung Injury in Neonatal Rats

Jia, Danyun; Zheng, Jinyu; Zhou, Yiyang; Jia, Jinqiu; Ye, Xiaoxiao; Zhou, Bingbing; Chen, Xingxing; Mo, Yunchang; Wang, Junlu

doi:10.2147/jir.s335061

Cited by 21 publications

(10 citation statements)

References 49 publications

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“…These studies suggested that rGSH served a protective role for the body through its redox function. in the present study, rGSH reduced the level of iron ions and acSl4 in aKi, and increased the expression of GPX4, thereby reducing the degree of kidney damage, which demonstrated that rGSH could ameliorate hemolytic aKi via regulation of the ferroptosis pathway, which was consistent with the results of previous studies that rGSH affects ferroptosis via regulation of the ferroptosis-related gene GPX4 (30). in the in vitro experiments, construction of the HK-2 cell ferroptosis model demonstrated that RGSH could significantly increase cell viability and significantly increase the lipid oxide level in cells, which inhibited cell apoptosis.…”

Section: Discussionsupporting

confidence: 93%

Reduced glutathione ameliorates acute kidney injury by inhibiting ferroptosis

Yuan

2023

Mol Med Rep

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Reduced glutathione (RGSH) can participate in the redox process in the body and inhibit damage to important organs caused by free radicals. Due to its broad biological effects, in addition to its clinical applications in treatment of liver diseases, RGSH is also used in the treatment of numerous other diseases, such as malignant tumors and nerve, urological and digestion diseases. However, there are few reports of RGSH being used in treatment of acute kidney injury (AKI), and the mechanism of its action in AKI is not clear. To assess the possible mechanism of RGSH inhibition in AKI, a mouse AKI model and HK-2 cell ferroptosis model were built to perform in vitro and in vivo experiments. The levels of blood urea nitrogen (BUN) and malondialdehyde (MDA) before and after the RGSH treatment were assessed, and the pathological changes of the kidneys were assessed using hematoxylin and eosin staining. Immunohistochemical (IHC) methods were used to evaluate the expressions of acyl-CoA synthetase long-chain family member 4 (ACSL4) and glutathione peroxidase (GPX4) in the kidney tissues, reverse transcription-quantitative PCR and western blotting were used to assess the levels of ferroptosis marker factors in the kidney tissues and HK-2 cells, and flow cytometry was used to assess cell death. The results indicated that, RGSH intervention reduced the BUN and serum MDA levels, and ameliorated glomerular damage and the level of renal structure damage in the mouse model. IHC results demonstrated that RGSH intervention could significantly reduce the ACSL4 mRNA expression level and inhibit iron accumulation, and significantly upregulate the GPX4 mRNA expression level. Moreover, RGSH could inhibit ferroptosis induced by ferroptosis inducers erastin and RSL3 in HK-2 cells. Cell assay results demonstrated that RGSH could improve the lipid oxide level and cell viability, and inhibit cell death, so as to ameliorate the effects of AKI. These results suggested that RGSH could ameliorate AKI by inhibiting ferroptosis, which indicates RGSH as a promising therapeutic strategy for the treatment of AKI.

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Section: Discussionsupporting

confidence: 93%

Reduced glutathione ameliorates acute kidney injury by inhibiting ferroptosis

Yuan

2023

Mol Med Rep

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“…Ferroptosis is a newly discovered form of cell death caused by the accumulation of iron-dependent lipid peroxides (LPOs) [51][52][53] that has recently been associated with immune responses in tumors. [54][55][56] Several studies have even described ferroptosis cell death as a form of ICD.…”

Section: Ferroptosismentioning

confidence: 99%

A mitochondria-localized iridium(iii) photosensitizer for two-photon photodynamic immunotherapy against melanoma

Chao

Wang

Karges³

et al. 2023

Chem. Sci.

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“…Next, we would like to explore the effects of the FHOD1‐HSPB1 signaling axis in the regulation of ferroptosis. As shown in Figure 5A, in T98G and U251 glioma cells, HSPB1 overexpression suppressed the FHOD1 knockdown‐mediated upregulation of TRF1, a ferroptosis‐positive regulator 34 . Moreover, overexpression of HSPB1 in FHOD1‐depleted glioma cells significantly reduced the inhibition of cell growth (Figure 5B,C).…”

Section: Resultsmentioning

confidence: 83%

FHOD1 is upregulated in glioma cells and attenuates ferroptosis of glioma cells by targeting HSPB1 signaling

Zhang

Feng

et al. 2023

CNS Neurosci Ther

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BackgroundAs a new type of regulatory cell death, ferroptosis has been proven to be involved in cancer pathogenesis and therapeutic response. However, the detailed roles of ferroptosis or ferroptosis‐associated genes in glioma remain to be clarified.MethodsHere, we performed the TMT/iTRAQ‐Based Quantitative Proteomic Approach to identify the differentially expressed proteins between glioma specimens and adjacent tissues. Kaplan–Meier survival was used to estimate the survival values. We also explored the regulatory roles of abnormally expressed formin homology 2 domain‐containing protein 1 (FHOD1) in glioma ferroptosis sensitivity.ResultsIn our study, FHOD1 was identified to be the most significantly upregulated protein in glioma tissues. Multiple glioma datasets revealed that the glioma patients with low FHOD1 expression displayed favorable survival time. Functional analysis proved that the knockdown of FHOD1 inhibited cell growth and improved the cellular sensitivity to ferroptosis in glioma cells T98G and U251. Mechanically, we found the up‐regulation and hypomethylation of HSPB1, a negative regulator of ferroptosis, in glioma tissues. FHOD1 knockdown could enhance the ferroptosis sensitivity of glioma cells via up‐regulating the methylated heat‐shock protein B (HSPB1). Overexpression of HSPB1 significantly reversed FHOD1 knockdown‐mediated ferroptosis.ConclusionsIn summary, this study demonstrated that the FHOD1‐HSPB1 axis exerts marked regulatory effects on ferroptosis, and might affect the prognosis and therapeutic response in glioma.

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Ferroptosis is Involved in Hyperoxic Lung Injury in Neonatal Rats

Cited by 21 publications

References 49 publications

Reduced glutathione ameliorates acute kidney injury by inhibiting ferroptosis

Reduced glutathione ameliorates acute kidney injury by inhibiting ferroptosis

A mitochondria-localized iridium(iii) photosensitizer for two-photon photodynamic immunotherapy against melanoma

FHOD1 is upregulated in glioma cells and attenuates ferroptosis of glioma cells by targeting HSPB1 signaling

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