Mitochondrial Reactive Oxygen Species and Lytic Programmed Cell Death in Acute Inflammation DOI Creative Commons
Sergio Rius‐Pérez, Salvador Pérez, Michel B. Tolédano

et al.

Antioxidants and Redox Signaling, Journal Year: 2023, Volume and Issue: 39(10-12), P. 708 - 727

Published: July 14, 2023

Significance: Redox signaling through mitochondrial reactive oxygen species (mtROS) has a key role in several mechanisms of regulated cell death (RCD), necroptosis, ferroptosis, pyroptosis, and apoptosis, thereby decisively contributing to inflammatory disorders. The mtROS apoptosis been extensively addressed, but their involvement necrotic-like RCD just started being elucidated, providing novel insights into the pathophysiology acute inflammation. Recent Advances: p53 together with drive necroptosis inflammation downregulation sulfiredoxin peroxiredoxin 3. Mitochondrial hydroorotate dehydrogenase is redox system regulation ferroptosis. In addition, noncanonical pathway, which generates Ragulator-Rag complex acts via mTORC1 promote gasdermin D oligomerization, triggers pyroptosis. Critical Issues: trigger positive feedback loops leading lytic conjunction necrosome, inflammasome, glutathione depletion, peroxidase 4 deficiency. Future Directions: precise mechanism membrane rupture ferroptosis contribution disorders are still unclear, will need further research. antioxidants may provide promising therapeutic approaches toward However, establishing doses windows action be required optimize potential, avoid potential adverse side effects linked blockade beneficial adaptive signaling. Antioxid. Signal. 39, 708-727.

Language: Английский

Ficolin B secreted by alveolar macrophage exosomes exacerbates bleomycin-induced lung injury via ferroptosis through the cGAS-STING signaling pathway DOI Creative Commons
Wu Xu, Yixia Jiang,

Rong Li

et al.

Cell Death and Disease, Journal Year: 2023, Volume and Issue: 14(8)

Published: Aug. 30, 2023

Pathogenesis exploration and timely intervention of lung injury is quite necessary as it has harmed human health worldwide for years. Ficolin B (Fcn B) a recognition molecule that can recognize variety ligands play an important role in mediating the cell cycle, immune response, tissue homeostasis lung. However, Fcn bleomycin (BLM)-induced obscure. This study aims to investigate sources its mechanism BLM-induced injury. WT, Fcna-/-, Fcnb-/- mice were selected construct model. Lung epithelial cells utilized Exosomes secreted from alveolar macrophages (AMs) applied by transporting B. Clinical data suggested M-ficolin (homologous was raised plasma interstitial disease (ILD) patients. In mouse model, macrophage-derived aggravated fibrosis. further promoted development autophagy ferroptosis. Remarkably, experiment results revealed transported AMs exosomes accelerated ferroptosis through activation cGAS-STING pathway. contrast, application 3-Methyladenine (3-MA) reversed promotion effect on damage inhibiting autophagy-dependent Meanwhile, facilitated fibrosis via summary, this demonstrated exacerbated promoting signaling

Language: Английский

Citations

27
Hypoxia and ferroptosis DOI Creative Commons
Xiaoqian Liu,

Meng-Zhen Shi,

Yuting Bai

et al.

Cellular Signalling, Journal Year: 2024, Volume and Issue: 122, P. 111328 - 111328

Published: Aug. 1, 2024

Ferroptosis is a novel, iron-dependent cell death characterized by the excessive accumulation of ferroptosis lipid peroxides ultimately leading to oxidative damage membrane. Iron, lipid, amino acid metabolism, and other signaling pathways all control ferroptosis. Numerous bodily tissues experience hypoxia under normal pathological circumstances. Tissue cells can adjust these changes activating hypoxia-inducible factor (HIF) pathway mechanisms in response hypoxic environment. In recent years, there has been increasing evidence that are closely linked, regulate specific conditions through different pathways. this paper, we review possible positive negative regulatory factors, as well ferroptosis-associated ischemic diseases, with intention delivering novel therapeutic avenues for defense management illnesses linked

Language: Английский

Citations

11
The protective effect of Lonicera japonica Thunb. against lipopolysaccharide-induced acute lung injury in mice: Modulation of inflammation, oxidative stress, and ferroptosis DOI
Lewen Xiong, Yan Liu, Yang Wang

et al.

Journal of Ethnopharmacology, Journal Year: 2024, Volume and Issue: 331, P. 118333 - 118333

Published: May 14, 2024

Language: Английский

Citations

9
Ferroptosis in Pulmonary Disease and Lung Cancer: Molecular Mechanisms, Crosstalk Regulation, and Therapeutic Strategies DOI Creative Commons
Dandan Guo, Songhua Cai,

Lvdan Deng

et al.

MedComm, Journal Year: 2025, Volume and Issue: 6(3)

Published: Feb. 23, 2025

Ferroptosis is a distinct form of iron-dependent programmed cell death characterized primarily by intracellular iron accumulation and lipid peroxidation. Multiple cellular processes, including amino acid metabolism, various signaling pathways, autophagy, have been demonstrated to influence the induction progression ferroptosis. Recent investigations elucidated that ferroptosis plays crucial role in pathogenesis pulmonary disorders, lung injury, chronic obstructive disease, fibrosis, asthma. increasingly recognized as promising novel strategy for cancer treatment. Various immune cells within tumor microenvironment, CD8+ T cells, macrophages, regulatory natural killer dendritic shown induce modulate process through regulation metabolism pathways. Conversely, can reciprocally alter metabolic environment, leading activation or inhibition functions, thereby modulating responses. This paper reviews molecular mechanism describes discusses connection between microenvironment diseases, development prospect their interaction treatment diseases.

Language: Английский

Citations

1
Alveolar macrophage-derived exosomal tRF-22-8BWS7K092 activates Hippo signaling pathway to induce ferroptosis in acute lung injury DOI
Weixi Wang, Lin Zhu, Huiting Li

et al.

International Immunopharmacology, Journal Year: 2022, Volume and Issue: 107, P. 108690 - 108690

Published: March 15, 2022

Language: Английский

Citations

38
Sevoflurane Induces Ferroptosis of Glioma Cells Through Activating the ATF4-CHAC1 Pathway DOI Creative Commons
Yingyi Xu, Na Zhang, Cheng Chen

et al.

Frontiers in Oncology, Journal Year: 2022, Volume and Issue: 12

Published: March 17, 2022

Objective To clarify the function and mechanisms of sevoflurane (Sev) on ferroptosis in glioma cells. Methods Different concentrations Sev were used to treat cells U87 U251. Ferroptosis inducer Erastin was incubate combined with ATF4 siRNA transfection treatment. CCK-8 assay colorimetric performed analyze cell viability Fe + concentration, respectively. The releases reactive oxygen species (ROS) determined by flow cytometry analysis. Transcriptional sequencing screen differential genes affected U251 mRNA protein expression ferroptosis-associated detected qRT-PCR Western blotting. Results could suppress viability, increase ROS levels downregulate GPX4, upregulate transferrin, ferritin, Beclin-1 a dose-dependent manner mitophagy-related gene activating transcription factor 4 (ATF4) identified be enhanced analyzed transcriptional sequencing. ChaC glutathione-specific gamma-glutamylcyclotransferase 1 (CHAC1), which is involved ferroptosis, downstream ATF4. Inhibition interrupt CHAC1 induced treatment obviously inhibited elevated 2+ promoted generation level increased Erastin-treated Moreover, interruption Sev-induced suppression reversed Erastin. Conclusions In summary, this study suggested that exposure-induced ATF4-CHAC1 pathway

Language: Английский

Citations

37
The Emerging Role of Ferroptosis in Sepsis DOI
Yanting Liu, Sichuang Tan,

Yongbin Wu

et al.

DNA and Cell Biology, Journal Year: 2022, Volume and Issue: 41(4), P. 368 - 380

Published: March 30, 2022

Ferroptosis is a novel form of cell death characterized by the iron-dependent accumulation lipid peroxides and different from other types death. The mechanisms ferroptosis are discussed in review, including System Xc-, Glutathione Peroxidase 4 pathway, Suppressor Protein 1 Dihydroorotate Dehydrogenase pathway. associated with occurrence various diseases, sepsis. Research recent years has displayed that involved sepsis development. Iron chelators can inhibit development improve survival rate septic mice. ferroptotic cells release damage-associated molecular patterns peroxidation, which further mediate inflammatory responses. inhibitors resist sepsis-induced multiple organ dysfunction inflammation. Finally, we reviewed ferroptosis, an biochemistry, morphology, major regulatory mechanisms, injuries caused Exploring relationship between may yield new treatment targets for

Language: Английский

Citations

32
Sevoflurane Postconditioning Attenuates Cerebral Ischemia-Reperfusion Injury by Inhibiting SP1/ACSL4-Mediated Ferroptosis DOI Creative Commons
Ning Lyu,

Xiaoyun Li

Human & Experimental Toxicology, Journal Year: 2023, Volume and Issue: 42

Published: Feb. 26, 2023

Sevoflurane is the most commonly used anesthetic in clinical practice and exerts a protective effect on cerebral ischemia-reperfusion (I/R) injury. This study aims to elucidate molecular mechanism by which sevoflurane postconditioning protects against I/R Oxygen-glucose deprivation/reperfusion (OGD/R) model vitro middle artery occlusion (MCAO) vivo were established simulate reduced neurological deficits, infarction, ferroptosis after Interestingly, significantly inhibited specificity protein 1 (SP1) expression MACO rats HT22 cells exposed OGD/R. SP1 overexpression attenuated neuroprotective effects of OGD/R-treated cells, evidenced cell viability, increased apoptosis, cleaved caspase-3 expression. Furthermore, chromatin immunoprecipitation luciferase experiments verified that bound directly ACSL4 promoter region increase its In addition, via SP1/ACSL4 axis. Generally, our describes an anti-ferroptosis injury downregulating SP1/ASCL4 These findings suggest novel sight for protection indicate potential therapeutic approach variety diseases.

Language: Английский

Citations

17
Dysregulated dendritic cells in sepsis: functional impairment and regulated cell death DOI Creative Commons

Liyu Zheng,

Yu Duan,

Peng-yi He

et al.

Cellular & Molecular Biology Letters, Journal Year: 2024, Volume and Issue: 29(1)

Published: May 30, 2024

Abstract Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Studies have indicated that immune plays central role in the pathogenesis of sepsis. Dendritic cells (DCs) play crucial emergence The major manifestations DCs septic state are abnormal functions and depletion numbers, which linked higher mortality vulnerability secondary infections Apoptosis most widely studied pathway number reduction DCs. In past few years, there has been surge studies focusing on regulated cell death (RCD). This emerging field encompasses various forms death, such necroptosis, pyroptosis, ferroptosis, autophagy-dependent (ADCD). Regulation DC’s RCD can serve possible therapeutic focus for treatment Throughout time, numerous tactics devised effectively implemented improve during sepsis progression, including modifying inhibiting DC death. this review, we provide an overview functional impairment states. Also, highlight recent advances targeting regulate following challenge. Graphical

Language: Английский

Citations

8
Dehydrocostus Lactone Attenuates Methicillin-Resistant Staphylococcus aureus-Induced Inflammation and Acute Lung Injury via Modulating Macrophage Polarization DOI Open Access
Yaxian Wu, Fengjuan Jiang, Gang Liu

et al.

International Journal of Molecular Sciences, Journal Year: 2021, Volume and Issue: 22(18), P. 9754 - 9754

Published: Sept. 9, 2021

Dehydrocostus lactone (DHL), a natural sesquiterpene isolated from the traditional Chinese herbs Saussurea lappa and Inula helenium L., has important anti-inflammatory properties used for treating colitis, fibrosis, Gram-negative bacteria-induced acute lung injury (ALI). However, effects of DHL on Gram-positive macrophage activation ALI remains unclear. In this study, we found that inhibited phosphorylation p38 MAPK, degradation IκBα, nuclear translocation NF-κB p65, but enhanced AMP-activated protein kinase (AMPK) expression Nrf2 HO-1 in lipoteichoic acid (LTA)-stimulated RAW264.7 cells primary bone-marrow-derived macrophages (BMDMs). Given critical role MAPK/NF-κB AMPK/Nrf2 signaling pathways balance M1/M2 polarization inflammation, speculated would also have an effect polarization. Further studies verified promoted M2 reduced M1 polarization, then resulted decreased inflammatory response. An vivo study revealed exhibited ameliorated methicillin-resistant Staphylococcus aureus (MRSA)-induced ALI. addition, treatment significantly pathway activated signaling, leading to accelerated switching MRSA-induced murine model. Collectively, these data demonstrated can promote phenotype via interfering as well activating vitro vivo. Our results suggested might be novel candidate diseases caused by bacteria.

Language: Английский

Citations

40