Neuroprotective Effect of Hydrogen Sulfide Subchronic Treatment Against TBI-Induced Ferroptosis and Cognitive Deficits Mediated Through Wnt Signaling Pathway DOI Creative Commons
Jie Chen, Zhennan Chen, Dongyu Yu

et al.

Cellular and Molecular Neurobiology, Journal Year: 2023, Volume and Issue: 43(8), P. 4117 - 4140

Published: Aug. 25, 2023

Abstract Emerging evidence shows that targeting ferroptosis may be a potential therapeutic strategy for treating traumatic brain injury (TBI). Hydrogen sulfide (H 2 S) has been proven to play neuroprotective role in TBI, but little is known about the effects of H S on TBI-induced ferroptosis. In addition, it reported Wnt signaling pathway can also actively regulate However, whether inhibits via after TBI remains unclear. this study, we first found addition alleviating neuronal damage and cognitive impairments, remarkably attenuated abnormal iron accumulation, decreased lipid peroxidation, improved expression glutathione peroxidase 4, demonstrating potent anti-ferroptosis action TBI. Moreover, Wnt3a or liproxstatin-1 treatment obtained similar results, suggesting activation render cells less susceptible post-TBI. More importantly, XAV939, an inhibitor pathway, almost inversed inactivation reduction loss caused by treatment, substantiating involvement S. conclusion, might critical mechanism realizing against Graphical induces ferroptosis-related changes characterized overload, impaired antioxidant system, peroxidation at chronic phase NaHS subchronic reduces susceptibility ferroptosis, least partly activating pathway.

Language: Английский

Ferroptosis: a new hunter of hepatocellular carcinoma DOI Creative Commons

Yulang Jiang,

Yongxin Yu,

Ziyang Pan

et al.

Cell Death Discovery, Journal Year: 2024, Volume and Issue: 10(1)

Published: March 13, 2024

Abstract Ferroptosis is an iron ion-dependent, regulatory cell death modality driven by intracellular lipid peroxidation that plays a key role in the development of HCC. Studies have shown various clinical agents (e.g., sorafenib) ferroptosis inducer-like effects and can exert therapeutic modulating different factors pathway. This implies targeting tumor may be very promising strategy for therapy. In this paper, we summarize prerequisites defense systems occurrence targets drug-mediated action HCC, differences connections between other programmed deaths. We aim to theoretical basis, classical inducers research progress HCC cells, clued treatment regulating network. Further investigation specific mechanisms hepatocellular carcinoma interventions at stages will help us deepen our understanding carcinoma, with view providing new more precise preventive as well measures patients.

Language: Английский

Citations

20
PM2.5-induced iron homeostasis imbalance triggers cardiac hypertrophy through ferroptosis in a selective autophagy crosstalk manner DOI Creative Commons
Tianyu Li, Mengqi Sun,

Qinglin Sun

et al.

Redox Biology, Journal Year: 2024, Volume and Issue: 72, P. 103158 - 103158

Published: April 12, 2024

Exposure to PM2.5 is correlated with cardiac remodeling, of which hypertrophy one the main clinical manifestations. Ferroptosis plays an important role in hypertrophy. However, potential mechanism PM2.5-induced through ferroptosis remains unclear. This study aimed explore molecular caused by and intervention MitoQ involved this process. The results showed that could induce dysfunction mice. Meanwhile, characteristics were observed, such as iron homeostasis imbalance, lipid peroxidation, mitochondrial damage abnormal expression key molecules. treatment effectively mitigate these alternations. After treating human cardiomyocyte AC16 PM2.5, activator (Erastin) inhibitor (Fer-1), it was found promote ferritinophagy lead well accumulation intracellular labile iron. Subsequently, mitophagy activated provided additional source iron, enhancing sensitivity cells ferroptosis. Furthermore, Fer-1 alleviated cytotoxicity overload cytoplasm mitochondria cells. It worth noting during process ferroptosis, metabolism mediated activation a temporal order. In addition, NCOA4 knockdown reversed imbalance peroxidation thereby alleviating summary, our imbalance-mediated crosstalk played

Language: Английский

Citations

17
Ferritinophagy Mediated by Oxidative Stress-Driven Mitochondrial Damage Is Involved in the Polystyrene Nanoparticles-Induced Ferroptosis of Lung Injury DOI
Sheng Yang, Tianyi Zhang, Yiling Ge

et al.

ACS Nano, Journal Year: 2023, Volume and Issue: 17(24), P. 24988 - 25004

Published: Dec. 12, 2023

Nanoplastics are a common type of contaminant in the air. However, no investigations have focused on toxic mechanism lung injury induced by nanoplastic exposure. In present study, polystyrene nanoplastics (PS-NPs) caused ferroptosis epithelial cells, which could be alleviated ferrostatin-1, deferoxamine, and N-acetylcysteine. Further investigation found that PS-NPs disturbed mitochondrial structure function triggered autophagy. Mechanistically, oxidative stress-derived damage contributed to ferroptosis, autophagy-dependent ferritinophagy was pivotal intermediate link, resulting ferritin degradation iron ion release. Furthermore, inhibition using ferrostatin-1 pulmonary systemic toxicity reverse mouse inhalation. Most importantly, lung-on-a-chip further used clarify role PS-NPs-induced visualizing stress, alveolar-capillary barrier dysfunction at organ level. summary, our study indicated an important for nanoplastics-induced through different inhalation models, three-dimensional-based lung-on-a-chip, providing insightful reference assessment nanoplastics.

Language: Английский

Citations

40
Association between ethylene oxide exposure and prevalence of COPD: Evidence from NHANES 2013–2016 DOI
Qiong Huang,

Siqi Li,

Jinfa Wan

et al.

The Science of The Total Environment, Journal Year: 2023, Volume and Issue: 885, P. 163871 - 163871

Published: May 4, 2023

Language: Английский

Citations

36
PM2.5 contributed to pulmonary epithelial senescence and ferroptosis by regulating USP3-SIRT3-P53 axis DOI
Ning Li, Rui Xiong, Guorui Li

et al.

Free Radical Biology and Medicine, Journal Year: 2023, Volume and Issue: 205, P. 291 - 304

Published: June 20, 2023

Language: Английский

Citations

32
Oxidative stress is the pivot for PM2.5-induced lung injury DOI

Tianhua Hou,

Laiyu Zhu,

Yusheng Wang

et al.

Food and Chemical Toxicology, Journal Year: 2023, Volume and Issue: 184, P. 114362 - 114362

Published: Dec. 13, 2023

Language: Английский

Citations

32
Scutellarein alleviates chronic obstructive pulmonary disease through inhibition of ferroptosis by chelating iron and interacting with arachidonate 15‐lipoxygenase DOI
Lu Liu, Yunsen Zhang, Lun Wang

et al.

Phytotherapy Research, Journal Year: 2023, Volume and Issue: 37(10), P. 4587 - 4606

Published: June 24, 2023

Abstract Ferroptosis, an iron‐dependent cell death characterized by lethal lipid peroxidation, is involved in chronic obstructive pulmonary disease (COPD) pathogenesis. Therefore, ferroptosis inhibition represents attractive strategy for COPD therapy. Herein, we identified natural flavonoid scutellarein as a potent inhibitor the first time, and its underlying mechanisms of COPD. In vitro, anti‐ferroptotic activity was investigated through CCK8, real‐time quantitative polymerase chain reaction (RT‐qPCR), Western blotting, flow cytometry, transmission electron microscope (TEM). vivo, induced lipopolysaccharide (LPS)/cigarette smoke (CS) assessed changes histopathological, inflammatory, ferroptotic markers. The were RNA‐sequencing (RNA‐seq), electrospray ionization mass spectra (ESI‐MS), local surface plasmon resonance (LSPR), drug affinity responsive target stability (DARTS), cellular thermal shift assay (CETSA), molecular dynamics. Our results showed that significantly inhibited Ras‐selective small molecule (RSL)‐3‐induced mitochondria injury BEAS‐2B cells, ameliorated LPS/CS‐induced mice. Furthermore, also repressed RSL‐3‐ or GPX4 down‐regulation, overactivation Nrf2/HO‐1 JNK/p38 pathways. Mechanistically, Fe 2+ elevation directly chelating . Moreover, bound to peroxidizing enzyme arachidonate 15‐lipoxygenase (ALOX15), which resulted unstable state catalysis‐related cluster. Additionally, ALOX15 overexpression partially abolished scutellarein‐mediated activity. findings revealed alleviated inhibiting via interacting with ALOX15, highlighted candidate treatment other ferroptosis‐related diseases.

Language: Английский

Citations

29
Nrf2-mediated redox balance alleviates LPS-induced vascular endothelial cell inflammation by inhibiting endothelial cell ferroptosis DOI Creative Commons
Huimin Hou,

Xiujiao Qin,

Gaokai Li

et al.

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: Feb. 9, 2024

Abstract Ferroptosis plays an important role in inflammation and oxidative stress. Whether ferroptosis is involved the of vascular endothelial cells its regulation mechanism remains unclear. We estimated correlation between serum iron ion levels index 33 patients with arteriosclerosis. In vitro, HUVECs or without ferrostatin-1 were exposed to Lipopolysaccharide. Corresponding cell models verify target signaling pathway. The results showed that had a significant positive N ratio, N/L, LDL level, LDL/HDL ( P < 0.05), negative L ratio 0.05) arteriosclerosis patients. inflammation. Ferrostatin-1 can rescue LPS-induced by decreasing HMGB1/IL-6/TNF-α expression. Nrf2 high expression could protect against activating GPX4/GSH system, inhibiting ferritinophagy, alleviating It also found key adaptive regulatory factor damage induced NOX4 activation. These findings indicated contributed pathogenesis mediating Nrf2-mediated redox balance may be therapeutic strategy diseases.

Language: Английский

Citations

14
SP2509 functions as a novel ferroptosis inhibitor by reducing intracellular iron level in vascular smooth muscle cells DOI Creative Commons

Yi He,

Xingbo Wang, Siqi Chen

et al.

Free Radical Biology and Medicine, Journal Year: 2024, Volume and Issue: 219, P. 49 - 63

Published: April 10, 2024

Previous studies have shown that ferroptosis of vascular smooth muscle cells (VSMCs) is involved in the development aortic dissection (AD) and histone methylation regulates this process. SP2509 acts as a specific inhibitor lysine-specific demethylase 1 (LSD1), which governs variety biological processes. However, effect on VSMC AD remains to be elucidated. This aim study was investigate role underlying mechanism SP2509-mediated ferroptosis. Here, mouse model established, significantly reduced levels H3K4me1 H3K4me2 (target SP2509) were found aortas mice. In VSMCs, treatment led dose-dependent increase levels. Furthermore, we provided equivalent protection ferrostatin-1 against ferroptosis, evidenced by increased cell viability, decreased death lipid peroxidation. RNA-sequencing analysis subsequent experiments revealed counteracted cystine deficiency-induced response inflammation oxidative stress. More importantly, demonstrated inhibited expression TFR ferritin reduce intracellular iron levels, thereby effectively blocking process Therefore, our findings indicate protects VSMCs from multiple stimulus-induced reducing preventing peroxidation death. These suggest may promising drug alleviate deposition

Language: Английский

Citations

12
Quercetin alleviates PM2.5-induced chronic lung injury in mice by targeting ferroptosis DOI Creative Commons
Shibin Ding, Jinjin Jiang, Li Yang

et al.

PeerJ, Journal Year: 2024, Volume and Issue: 12, P. e16703 - e16703

Published: Jan. 2, 2024

Background PM 2.5 is a well-known harmful air pollutant that can lead to acute exacerbation and aggravation of respiratory diseases. Although ferroptosis involves in the pathological process pulmonary disease, potential mechanism -caused lung inflammation fibrosis need be further clarified. Quercetin phenolic compound inhibit various Hence, this study explores role injury induced by order elucidate beneficial effect quercetin its underlying mechanism. Methods C57BL/6J mice were treated with either saline or intratracheal instillation 20 times (once every two days). Additionally, -treated supplemented doses quercetin. Lung injury, lipid peroxidation, iron content marker protein expression Nrf2 signaling pathway evaluated. In vitro , cell experiments applied verify mechanisms links between activation as well inflammation. Results vivo increased caused peroxidation contents, contents markers tissues; these effects significantly reversed upregulated nuclear downregulated Keap1 tissues -exposed mice. decreased products, levels translocation degradation BEAS-2B cells. Moreover, we found dimethyl fumarate markedly production activating Nrf2-Keap1 Furthermore, reduced inflammatory cytokines TGF- β 1 Conclusion Our data suggested involved -induced alleviate adverse via pathway.

Language: Английский

Citations

10