Abstract:Ferroptosis, a type of cell death involving iron and lipid peroxidation, has been found to be closely associated with the development of many diseases. Mitochondria are vital components of eukaryotic cells, serving important functions in energy production, cellular metabolism, and apoptosis regulation. Presently, the precise relationship between mitochondria and ferroptosis remains unclear. In this study, we aim to systematically elucidate the mechanisms via which mitochondria regulate ferroptosis from multipl… Show more
“…Contemporary research underscores the connection between mitochondria and lung cancer, thereby establishing it as a pivotal factor influencing the initiation and progression of lung cancer. Inhibition of mitochondrial function has demonstrated the potential to impede the onset and proliferation of lung cancer [ 23 , 24 ].…”
“…Contemporary research underscores the connection between mitochondria and lung cancer, thereby establishing it as a pivotal factor influencing the initiation and progression of lung cancer. Inhibition of mitochondrial function has demonstrated the potential to impede the onset and proliferation of lung cancer [ 23 , 24 ].…”
“…In our study, we constructed a novel 4-gene risk model associated with disulfidptosis based on a combination of the DRGs and scRNA sequencing data of papillary thyroid carcinoma. As a newly discovered type of programmed cell death, disulfidptosis is considered to be closely related to the occurrence and development of tumors as ferroptosis and cuproptosis death which were fully explored in the past ( Feng et al, 2023 ; Hadian and Stockwell, 2023 ; Zhang et al, 2023 ). In-depth exploration of these cell death processes will help us to deepen our understanding of the mechanisms behind tumor development and provide evidence for investigating new treatments.…”
Background: Disulfidptosis is a newly discovered form of regulated cell death. The research on disulfidptosis and tumor progression remains unclear. Our research aims to explore the relationship between disulfidptosis-related genes (DRGs) and the clinical outcomes of papillary thyroid carcinoma (PTC), and its interaction on the tumor microenvironment.Methods: The single-cell RNA seq data of PTC was collected from GEO dataset GSE191288. We illustrated the expression patterns of disulfidptosis-related genes in different cellular components in thyroid cancer. LASSO analyses were performed to construct a disulfidptosis associated risk model in TCGA-THCA database. GO and KEGG analyses were used for functional analyses. CIBERSORT and ESTIMATE algorithm helped with the immune infiltration estimation. qRT‒PCR and flow cytometry was performed to validate the hub gene expression and immune infiltration in clinical samples.Results: We clustered PTC scRNA seq data into 8 annotated cell types. With further DRGs based scoring analyses, we found endothelial cells exhibited the most relationship with disulfidptosis. A 4-gene risk model was established based on the expression pattern of DRGs related endothelial cell subset. The risk model showed good independent prognostic value in both training and validation dataset. Functional enrichment and genomic feature analysis exhibited the significant correlation between tumor immune infiltration and the signature. The results of flow cytometry and immune infiltration estimation showed the higher risk scores was related to immuno-suppressive tumor microenvironment in PTC.Conclusion: Our study exhibited the role of disulfidptosis based signature in the regulation of tumor immune microenvironment and the survival of PTC patients. A 4-gene prognostic signature (including SNAI1, STC1, PKHD1L1 and ANKRD37) was built on the basis of disulfidptosis related endothelial cells. The significance of clinical outcome and immune infiltration pattern was validated robustly.
“…Additionally, it differs from other regulated cell deaths in terms of its morphology and underlying mechanisms. Diverse processes, including iron, energy, lipid metabolisms, and specific small molecules, influence the course of ferroptosis and the susceptibility of cells to the process ( Feng et al, 2023 ). Given the emerging understanding of ferroptosis, it has been implicated in the pathogenesis of malaria.…”
Ferroptosis is an iron-dependent form of regulated cell death characterized by glutathione (GSH) depletion, glutathione peroxidase 4 (GPX4) inactivation, and the build-up of lipotoxic reactive species. Ferroptosis-targeted induction is a promising therapeutic approach for addressing antimalarial drug resistance. In addition to being the primary source of intracellular energy supply and reactive oxygen species (ROS) generation, mitochondria actively participate in diverse forms of regulated cell death, including ferroptosis. Altered mitochondrial morphology and functionality are attributed to ferroptosis. Diverse mitochondria-related proteins and metabolic activities have been implicated in fine-tuning the action of ferroptosis inducers. Herein, we review recent progress in this evolving field, elucidating the numerous mechanisms by which mitochondria regulate ferroptosis and giving an insight into the role of the organelle in ferroptosis. Additionally, we present an overview of how mitochondria contribute to ferroptosis in malaria. Furthermore, we attempt to shed light on an inclusive perspective on how targeting malaria parasites’ mitochondrion and attacking redox homeostasis is anticipated to induce ferroptosis-mediated antiparasitic effects.
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