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468 results for “ferroptosis”
OMA1-mediated integrated stress response protects against ferroptosis in mitochondrial cardiomyopathy
<p>Cardiomyopathy and heart failure are common manifestations in mitochondrial disease caused by deficiencies in the oxidative phosphorylation system of mitochondria (OXPHOS). Here, we demonstrate that the cardiac-specific loss of the assembly factor Cox10 of the cytochrome <em>c</em> oxidase causes mitochondrial cardiomyopathy in mice, which is associated with OXPHOS deficiency, lysosomal defects and an aberrant mitochondrial morphology. Activation of the mitochondrial peptidase Oma1 in <em>Cox10</em><sup>-/-</sup> mice results in mitochondrial fragmentation and induction of the integrated stress response (ISR) along the Oma1-Dele1-Atf4 signalling axis. Ablation of <em>Oma1</em> or <em>Dele1</em> in <em>Cox10</em><sup>-/-</sup> mice aggravates cardiomyopathy. ISR inhibition impairs the cardiac glutathione metabolism, limits the selenium-dependent accumulation of the glutathione peroxidase Gpx4 and increases lipid peroxidation in the heart, ultimately culminating in ferroptosis. Our results demonstrate a protective role of the Oma1-Dele1-mediated ISR in mitochondrial cardiomyopathy and link ferroptosis to OXPHOS deficiency and mitochondrial disease.</p>
Identifying a novel ferroptosis-related prognostic score for predicting prognosis in chronic lymphocytic leukemia
<p><span><strong>Background</strong>:</span><span> Chronic lymphocytic leukemia (CLL) is the most common leukemia in the western world. Although the treatment landscape for CLL is rapidly evolving, there are still some patients who remain drug resistance or disease refractory. Ferroptosis is a type of lipid peroxidation-induced cell death and has been suggested with a prognostic value in several cancers. Our research aims to build a prognostic model to improve risk stratification in CLL patients and facilitate more accurate assessment for clinical management.</span></p> <p><span><strong>Methods</strong>: </span><span>The differentially expressed ferroptosis-related genes (</span><span>FRGs) in CLL were filtered through univariate Cox regression analysis based on public databases. Least Absolute Shrinkage and Selection Operator (LASSO) Cox algorithms were performed to construct a prognostic risk model. CIBERSORT and single-sample gene set enrichment analysis (ssGSEA) were performed to estimate the immune infiltration score and immune-related pathways. A total of thirty-six CLL patients in our center were enrolled in this study as a validation cohort. Moreover, a nomogram model was established to predict the prognosis.</span></p> <p><span><strong>Results</strong>: </span><span>A total of differentially expressed 15 FRGs with prognostic significance were screened out. After minimizing the potential risk of overfitting, we constructed a novel ferroptosis-related prognostic score (FPS) model with nine FRGs (AKR1C3, BECN1, CAV1, CDKN2A, CXCL2, JDP2, SIRT1, SLC1A5 and SP1), and stratified patients into low-risk and high-risk groups. Kaplan–Meier analysis showed that patients with high FPS had worse overall survival (OS) (P<0.0001) and treatment-free survival (TFS) (P<0.0001). ROC curves evaluated the prognostic prediction ability of the FPS model. Additionally, the immune cell types and immune-related pathways were correlated with the risk scores in CLL patients. In the validation cohort, the results confirmed </span><span>that the </span><span>high</span><span>-</span><span>risk group was related to worse OS (P<0.0001), progress-free survival (PFS) (P=0.0140) and TFS (P=0.0072). </span><span>In</span><span> the multivariate analysis, only FPS (P=0.011) and CLL-IPI (P=0.010) were independent risk indicators for OS. Furthermore, we established a nomogram including FPS and CLL-IPI which could strongly and reliably predict individual prognosis.</span></p> <p><span><strong>Conclusion</strong>: </span><span>A novel FPS model could be used in CLL for prognostic prediction. The model index may also facilitate the development of new clinical ferroptosis-targeted therapies in patients with CLL.</span></p>
Identifying a novel ferroptosis-related prognostic score for predicting prognosis in chronic lymphocytic leukemia
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Gut microbiota-derived gamma-aminobutyric acid from metformin treatment reduces hepatic ischemia/reperfusion injury by inhibiting ferroptosis
<div>Hepatic ischemia/reperfusion injury (HIRI) is a common and inevitable factor leading to poor prognosis in various liver diseases, making the outcomes of current treatments in the clinic unsatisfactory. Metformin has been demonstrated to be beneficial in alleviating HIRI in recent studies, however, the underpinning mechanism remains unclear. In this study, we found metformin mitigates HIRI-induced ferroptosis through reshaped gut microbiota in mice, which was confirmed by the results of fecal microbiota transplantation treatment but showed the elimination of the beneficial effects when gut bacteria were depleted using antibiotics. Detailedly, through 16S rRNA and metagenomic sequencing, we identified that the metformin-reshaped microbiota was characterized by the increase of gamma-aminobutyric acid (GABA) producing bacteria. This increase was further confirmed by the elevation of GABA synthesis key enzymes, glutamic acid decarboxylase, and putrescine aminotransferase, in gut microbes of metformin-treated mice and healthy volunteers. Furthermore, the benefit of GABA against HIRI-induced ferroptosis was demonstrated in GABA-treated mice. Collectively, our data indicate that metformin can mitigate HIRI-induced ferroptosis by reshaping gut microbiota, with GABA identified as a key metabolite.</div>
Supplementary Materials for Evaluation role of ferroptosis long non-coding RNAs for immune microenvironment and microsatellite instability in colon cancer
<p>Supplementary Materials for "Evaluation role of ferroptosis long non-coding RNAs for immune microenvironment and microsatellite instability in colon cancer"</p>
Fig. 6. C3 activated the Nrf2 in Triterpenoids from Uncaria macrophylla as ferroptosis inhibitors
Fig. 6. C3 activated the Nrf2/SLC7A11/GPx4 axis. (A) C3 increased the protein levels of Nrf2, SLC7A11 and GPx4 in a dose-dependent manner. (B) ML385 treatment abolished the neuroprotective effect of C3 in PC12 cells. (C) ML385 blocked the activation of Nrf2, SLC7A11 and GPx4.
Fig. 4. 13C in Triterpenoids from Uncaria macrophylla as ferroptosis inhibitors
Fig. 4. 13C NMR calculation results of 5 and 6. (A) Linear regression analysis of calculated 13C NMR shifts of 2′R (left) and 2′S (right) against the experimental shifts of 5 and the sDP4 probability for assignment of 5 to the candidate stereoisomers. (B) Linear regression analysis of calculated 13C NMR shifts of 2′R (left) and 2′S + (right) against the experimental shifts of 6 and the sDP4+ probability for assignment of 6 to the candidate stereoisomers.
Fig. 2. 1H–1H in Triterpenoids from Uncaria macrophylla as ferroptosis inhibitors
Fig. 2. 1H–1H COSY (red, bold) and selected HMBC (blue, arrows) correlations of 1–7. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 5 in Triterpenoids from Uncaria macrophylla as ferroptosis inhibitors
Fig. 5. Anti-ferroptosis activity of 1–7. (A) The neuroprotective effect of 1–7 in PC12 cells. (B) EC50 values of 2, 3 and 7. (C) C3 inhibited erastin-induced PC12 cells damage. Scale bar, 50 μm. (D) C3 suppressed erastin-induced ROS accumulation in PC12 cells. (E) C3 suppressed MDA accumulation in PC12 cells. Data were expressed as the mean ± SEM. ###P <0.001, ##P <0.01 vs control group. ***P <0.001, **P <0.01, *P <0.05 vs erastin group.
Ferroptosis in Patients With COPD COPD With/Without Risk of Cardiovascular Events. Pathophysiological Implications, Diagnostics and Prognoses. FerrEPOC Study.
ClinicalTrials.gov study NCT06102993. IPD Sharing: NO. Countries: 1. Publications: 0.
Gut microbiota-derived gamma-aminobutyric acid from metformin treatment reduces hepatic ischemia/reperfusion injury by inhibiting ferroptosis
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Esterase- responsive SLC7A11 shRNA Delivery System Induced Ferroptosis and Suppressed Hepatocellular Carcinoma Progression
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CellDeathPred: a deep learning framework for ferroptosis and apoptosis prediction based on cell painting
<p><strong>Data Description:</strong></p> <ul> <li>Two cell death modalities are considered in this study: apoptosis and ferroptosis. The treatments and their cell death types used in these experiments are shown in Figure 1 in the paper. In total we have seven apoptosis and seven ferroptosis inducers. They target specific cell organelles and components. Besides, active treatments there are negative controls DMSO and untreated wells.</li> <li>Every image has a resolution of 1360 x 1024. These four channels were imaged in the experiments. For every well multiple images (fields) are taken typically ten fields.</li> <li>Three plates with four different settings were imaged. 20x non-confocal (very fast [1.5h]), 20x confocal (fast [2.5h]), 40x non-confocal (slow [5h]), 40x confocal (very slow [8h]). All for one time point 28h (incubation time).</li> </ul>
Source code for ferroptosis gene set activity analysis in BLCA epithelial cells
<p>Source code for ferroptosis gene set activity analysis in BLCA epithelial cells </p>
The correlation between hippocampal ferroptosis and emotional disorders induced by neuropathic pain in CCI rats
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Icariin inhibits lung adenocarcinoma progression through TP53-mediated ferroptosis
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Fig. 3 in Triterpenoids from Uncaria macrophylla as ferroptosis inhibitors
Fig. 3. Key NOESY or ROESY correlations of 1–7.
Fig. 1 in Triterpenoids from Uncaria macrophylla as ferroptosis inhibitors
Fig. 1. Structures of compounds 1–7.
Human Hematopoietic Stem Cell Vulnerability to Ferroptosis
GEO Series GSE221170. Homo sapiens. 8 samples. Type: Expression profiling by high throughput sequencing; Other.
A cell state specific metabolic vulnerability to GPX4-dependent ferroptosis in glioblastoma
GEO Series GSE224727. Homo sapiens; Mus musculus. 34 samples. Type: Expression profiling by high throughput sequencing.
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