TSPO Exacerbates Sepsis-Induced Cardiac Dysfunction by Inhibiting p62-Mediated Autophagic Flux via the ROS-RIP1/RIP3-Exosome Axis DOI
Qiao Guo,

Haitang Liao,

Shuai Hao

и другие.

Free Radical Biology and Medicine, Год журнала: 2024, Номер 226, С. 56 - 69

Опубликована: Ноя. 13, 2024

Язык: Английский

Research progress on ferroptosis and PARP inhibitors in ovarian cancer: action mechanisms and resistance mechanisms DOI Creative Commons
Jiqing Zhang, Dan Ouyang, Mu Liu

и другие.

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Апрель 24, 2025

Ovarian cancer, a gynecologic malignancy with high mortality rates, faces persistent therapeutic challenges due to acquired resistance and frequent recurrence conventional therapies. While poly (ADP-ribose) polymerase (PARP) inhibitors have primarily transformed clinical outcomes through the synthetic lethality mechanism, their long-term efficacy remains constrained by resistance. Ferroptosis, novel programmed cell death modality characterized iron-dependent lipid peroxidation, has emerged as promising frontier in oncology. This review is first summarize mechanisms of action associated both ferroptosis PARP ovarian cancer.

Язык: Английский

Процитировано

0

Ferroptosis targeting offers a Therapeutic Target for Septic cardiomyopathy DOI
Ping Zhou, Mengxue Liu, Tao Lv

и другие.

Tissue and Cell, Год журнала: 2025, Номер 95, С. 102930 - 102930

Опубликована: Апрель 25, 2025

Язык: Английский

Процитировано

0

Mitochondrial quality control and transfer communication in neurological disorders and neuroinflammation DOI Creative Commons

Yinrui Ma,

Rui Song, Chenyang Duan

и другие.

Frontiers in Immunology, Год журнала: 2025, Номер 16

Опубликована: Апрель 28, 2025

Mitochondria, as the primary energy factories of cells, play a pivotal role in maintaining nervous system function and regulating inflammatory responses. The balance mitochondrial quality control is critical for neuronal health, disruptions this are often implicated pathogenesis various neurological disorders. Mitochondrial dysfunction not only exacerbates deficits but also triggers neuroinflammation through release damage-associated molecular patterns (DAMPs), such DNA (mtDNA) reactive oxygen species (ROS). This review examines mechanisms recent advancements diseases, focusing on processes fusion fission, mitophagy, biogenesis, protein expression regulation. It further explores subsequent cascades conditions ischemic hemorrhagic stroke, neurodegenerative diseases brain tumors. Additionally, emerging research highlights significance transfer mechanisms, particularly intercellular between neurons glial potential strategy mitigating inflammation promoting cellular repair. provides insights into underpinnings neuroinflammatory pathologies while underscoring translational targeting therapeutic development.

Язык: Английский

Процитировано

0

Hyperoside alleviates zearalenone-induced liver injury by regulating mitochondrial calcium overload mediated excessive autophagy DOI
Tianyu Han, Lulu Wang, Yan Jiang

и другие.

Phytomedicine, Год журнала: 2025, Номер unknown, С. 156880 - 156880

Опубликована: Май 1, 2025

Язык: Английский

Процитировано

0

Exploring Ferroptosis-Associated Gene Signatures as Diagnostic and Therapeutic Targets for Sepsis-Induced Cardiomyopathy DOI Open Access

Haobin Huang,

Chenbo Ge,

Yawei Dai

и другие.

Cureus, Год журнала: 2024, Номер unknown

Опубликована: Май 16, 2024

Background: Sepsis-induced cardiomyopathy (SICM) is a severe complication of sepsis associated with high mortality rates. Despite its significance, the molecular mechanisms underlying SICM remain poorly understood, particularly role ferroptosis - form iron-dependent programmed cell death. Methodology: This study analyzed GSE79962 dataset from Gene Expression Omnibus, containing cardiac gene expression profiles patients and controls. A list ferroptosis-related genes (FRGs) was retrieved FerrDb. We used limma package in R for differential analysis, setting an adjusted P-value cutoff <0.05 log2-fold change threshold ±1 to identify differentially expressed (DE-FRGs). applied machine learning algorithms biomarker identification, including least absolute shrinkage selection operator (LASSO) logistic regression support vector recursive feature elimination (SVM-RFE), implemented via glmnet e1071 packages R, respectively. set enrichment analysis (GSEA) conducted using GSEA investigate biological pathways related key DE-FRGs. Results: After we identified 145 Functional analyses underscored involvement these critical processes pathways, such as lipid metabolism insulin resistance. Machine approaches pinpointed five DE-FRGs (NCOA4, GABARAPL1, GJA1, CISD1, CP), strong predictive potential SICM. Further analyses, construction ceRNA network, revealed intricate post-transcriptional regulatory that may influence genes. Conclusions: Our findings highlight central biomarkers therapeutic targets could help refine diagnostic treatment strategies. advances our understanding underpinnings sets stage future research aimed at mitigating this complication.

Язык: Английский

Процитировано

3

The miR-182-5p/GPX4 Pathway Contributes to Sevoflurane-Induced Ototoxicity via Ferroptosis DOI Open Access

Lin Jin,

Xiaopei Yu,

Xuehua Zhou

и другие.

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(12), С. 6774 - 6774

Опубликована: Июнь 20, 2024

Our study aimed to investigate the role of ferroptosis in sevoflurane-induced hearing impairment and explore mechanism microRNA-182-5p (miR-182-5p)/Glutathione Peroxidase 4 (GPX4) pathway ototoxicity. Immunofluorescence staining was performed using myosin 7a CtBP2. Cell viability assessed CCK-8 kit. Fe2+ concentration measured FerroOrange Mi-to-FerroGreen fluorescent probes. The lipid peroxide level BODIPY 581/591 C11 MitoSOX auditory brainstem response (ABR) test conducted evaluate status. Bioinformatics tools dual luciferase gene reporter analysis were used confirm direct targeting miR-182-5p on GPX4 mRNA. expression cells by qRT-PCR Western blot. Ferrostatin-1 (Fer-1) pretreatment significantly improved damage ribbon synapses mice caused sevoflurane exposure. revealed that Fer-1 reduced intracellular mitochondrial iron overload, as well accumulation. findings indicated upregulated sevoflurane-exposed HEI-OC1 cells, regulated binding 3′UTR inhibition attenuated overload elucidated miR-182-5p/GPX4 implicated ototoxicity promoting ferroptosis.

Язык: Английский

Процитировано

1

Fighting ischemia-reperfusion injury: Focusing on mitochondria-derived ferroptosis DOI
Lei Tian, Qian Liu, Hong Guo

и другие.

Mitochondrion, Год журнала: 2024, Номер 79, С. 101974 - 101974

Опубликована: Окт. 24, 2024

Язык: Английский

Процитировано

1

FTMT-dependent mitophagy is crucial for ferroptosis resistance in cardiac fibroblast DOI

Cheng‐Zhang Xu,

Qing‐Yuan Gao,

Guang-Hao Gao

и другие.

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Год журнала: 2024, Номер 1871(8), С. 119825 - 119825

Опубликована: Авг. 19, 2024

Язык: Английский

Процитировано

0

TSPO Exacerbates Sepsis-Induced Cardiac Dysfunction by Inhibiting p62-Mediated Autophagic Flux via the ROS-RIP1/RIP3-Exosome Axis DOI
Qiao Guo,

Haitang Liao,

Shuai Hao

и другие.

Free Radical Biology and Medicine, Год журнала: 2024, Номер 226, С. 56 - 69

Опубликована: Ноя. 13, 2024

Язык: Английский

Процитировано

0