Nature Cell Biology, Journal Year: 2025, Volume and Issue: unknown
Published: June 5, 2025
Language: Английский
ACS Nano, Journal Year: 2025, Volume and Issue: unknown
Published: April 3, 2025
Disulfidptosis and ferroptosis are recently identified programmed cell deaths for tumor therapy, both of which highly depend on the intracellular cystine/cysteine transformation cystine transporter solute carrier family 7 member 11/glutathione/glutathione peroxidase 4 (SLC7A11/GSH/GPX4) antioxidant axis. However, disulfidptosis usually asynchronous due to opposite effect transport them. Herein, systematic glucose deprivation, by inhibiting upstream uptake promoting downstream consumption, is proposed synchronously evoke ferroptosis. As an example, Au nanodots Fe-apigenin (Ap) complexes coloaded FeOOH nanoshuttles (FeOOH@Fe-Ap@Au NSs) employed regulate SLC7A11/GSH/GPX4 axis performing disulfidptosis- ferroptosis-mediated therapy synchronously. In this scenario, exhibit oxidase-like activity when consuming massive glucose. Meanwhile, Ap can inhibit downregulating 1, depriving fundamentally. The systematical deprivation limits supplement NADPH suppresses axis, thus solving contradiction addition, efficient delivery exogenous iron ions FeOOH@Fe-Ap@Au NSs self-supplied H2O2 through nanodots-catalytic oxidation facilitate Fenton reaction therewith help amplify a result synchronous occurrence ferroptosis, good efficacy in ovarian cancer therapeutic model.
Language: Английский
Citations
2
Current Biology, Journal Year: 2025, Volume and Issue: 35(7), P. R241 - R243
Published: April 1, 2025
Language: Английский
Citations
1
Molecular Cancer, Journal Year: 2025, Volume and Issue: 24(1)
Published: May 3, 2025
Pyroptosis is a distinct form of programmed cell death characterized by the rupture membrane and robust inflammatory responses. Increasing evidence suggests that pyroptosis significantly affects tumor microenvironment antitumor immunity releasing damage-associated molecular patterns (DAMPs) pro-inflammatory mediators, thereby establishing it as pivotal target in cancer immunotherapy. This review thoroughly explores mechanisms underlying pyroptosis, with particular focus on inflammasome activation gasdermin family proteins (GSDMs). It examines role pyroptotic reshaping immune (TIME) involving both cells, discusses recent advancements targeting pathways through therapeutic strategies such small molecule modulators, engineered nanocarriers, combinatory treatments checkpoint inhibitors. We also advances future directions to enhance immunotherapy inhibitors, adoptive therapy, vaccines. study suggested offers promising avenue amplify responses surmount resistance existing immunotherapies, potentially leading more efficacious treatments.
Language: Английский
Citations
1
Molecular Cancer, Journal Year: 2025, Volume and Issue: 24(1)
Published: May 7, 2025
Cancer immunotherapy, encompassing both experimental and standard-of-care therapies, has emerged as a promising approach to harnessing the immune system for tumor suppression. Experimental strategies, including novel immunotherapies preclinical models, are actively being explored, while established treatments, such checkpoint inhibitors (ICIs), widely implemented in clinical settings. This comprehensive review examines historical evolution, underlying mechanisms, diverse strategies of cancer highlighting its applications ongoing advancements. The delves into essential components anticancer immunity, dendritic cell activation, T priming, surveillance, addressing challenges posed by evasion mechanisms. Key immunotherapeutic vaccines, oncolytic viruses, adoptive transfer, ICIs, discussed detail. Additionally, role nanotechnology, cytokines, chemokines, adjuvants enhancing precision efficacy were explored. Combination particularly those integrating immunotherapy with radiotherapy or chemotherapy, exhibit synergistic potential but necessitate careful management reduce side effects. Emerging factors influencing outcomes, heterogeneity, gut microbiota composition, genomic epigenetic modifications, also examined. Furthermore, molecular mechanisms therapeutic resistance analyzed, focus on contributions noncoding RNAs alterations, along innovative intervention strategies. emphasizes recent advancements, particular attention biomarker-driven approaches aimed at optimizing patient prognosis. Challenges immunotherapy-related toxicity, limited solid tumors, production constraints highlighted critical areas future research. Advancements personalized therapies delivery systems proposed avenues enhance treatment effectiveness accessibility. By incorporating insights from multiple disciplines, this aims deepen understanding application ultimately fostering more effective accessible solutions.
Language: Английский
Citations
1
Journal of Colloid and Interface Science, Journal Year: 2025, Volume and Issue: 685, P. 509 - 521
Published: Jan. 14, 2025
Language: Английский
Citations
0
Advanced Science, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 10, 2025
Abstract Cuproptosis is a newly discovered copper‐dependent form of cell death. Intracellular glutathione (GSH) acts as copper chelator to inhibit cuproptosis, so the reduction GSH concentration conducive enhancing cuproptosis cells. In order reduce content and interfere with mitochondrial metabolism, strategy based on calcium overload depletion enhance proposed in this study. Containing manganese (Mn) (Cu) elements, CaCO 3 nanoparticles (NPs) are modified MCF‐7 aptamer (CaCO /Mn/Cu@lip‐Apt). When entering cell, /Mn/Cu@lip‐Apt decomposed released Mn* (Mn 2+ /Mn 3+ 4+ ), Cu Ca . The high valence Mn ion can effectively consume produce which catalyzed H 2 O reactive oxygen species (ROS), while reducing concentration. production ROS promoted influx exogenous large accumulation led intracellular overload, resulting dysfunction metabolism disorders. , turn triggered cuproptosis. This showed excellent antitumor effects provided new way study disease treatment.
Language: Английский
Citations
0
Frontiers in Neuroscience, Journal Year: 2025, Volume and Issue: 19
Published: March 5, 2025
Disulfidptosis is a pathologic process that occurs under conditions of NADPH deficiency and excess disulfide bonds in cells express high levels SLC7A11. This caused by glucose deprivation-induced stress was first described cancer researchers. Oxidative hypothesized mechanism underlying diseases the central nervous system (CNS), specific type oxidative stress. Proteins linked to disulfidptosis metabolic pathways involved are significantly associated with CNS (neurodegenerative disease, neurogliomas ischemic stroke). However, responsible for this correlation remains unknown. review provides comprehensive overview current knowledge regarding origin elements, genetic factors, signaling proteins pathogenesis disulfidptosis. It demonstrates disruption thiometabolism play critical roles diseases, which potential role We also summarize disulfidptosis-related drugs highlight therapeutic strategies treating diseases. Additionally, paper suggests testable hypothesis might be promising target
Language: Английский
Citations
0
Journal of Colloid and Interface Science, Journal Year: 2025, Volume and Issue: unknown, P. 137381 - 137381
Published: March 1, 2025
Language: Английский
Citations
0
Journal of Advanced Research, Journal Year: 2025, Volume and Issue: unknown
Published: March 1, 2025
Ferroptosis represents a promising therapeutic approach for breast cancer treatment. However, cells can develop resistance through the SLC7A11-GSH-GPX4 axis, wherein increased SLC7A11 expression enhances cystine uptake, replenishes GSH, and reactivates GPX4. Notably, with high become vulnerable to disulfidptosis under glucose-deprived conditions. We aimed dual-mode strategy that simultaneously induces ferroptosis by targeting both lipid peroxidation glucose metabolism in cells. Fe-Cu-SS metal-organic frameworks (MOFs) loaded BAY876 (FCSP@876 MOFs) were synthesized enhance trigger The MOFs characterized using transmission electron microscopy (TEM), Fourier-transform infrared (FTIR) spectroscopy, X-ray photoelectron spectroscopy (XPS), UV-Vis spectroscopy. In vitro experiments demonstrated FCSP@876 reactive oxygen species (ROS) levels while depleting NADPH. Western blotting actin filament staining confirmed underlying mechanisms. vivo xenograft BALB/c mice assessed synergistic effects of induction. During induction, exhibited an adaptive upregulation expression. effectively counteracted this mechanism inducing restricting uptake BAY876, leading NADPH depletion subsequent disulfidptosis. Both enhanced efficacy compared single-mode treatments. This study successfully developed novel combines MOFs, offering overcoming therapy.
Language: Английский
Citations
0
ACS Applied Materials & Interfaces, Journal Year: 2025, Volume and Issue: unknown
Published: April 1, 2025
Tumor remains a leading contributor to global mortality rates, necessitating urgent advancements in therapeutic interventions. Due the intricate nature of tumor microenvironment, individual differences make it difficult achieve desired efficacy with single strategy. To overcome these challenges, we develop for first time hollow NaBiF4-based nanocomposites NaBiF4-W/R-D therapy by glucose transporter 1 (GLUT1) inhibition and mitochondrial function disruption. can inhibit GLUT1 due presence WZB117, which leads decrease intracellular cells, leaving them starved state. Meanwhile, upconversion luminescence under near-infrared (NIR) laser irradiation stimulate photosensitizer efficiently generate singlet oxygen disrupt then kill cells. In addition, NIR-II emission from is used fluorescence imaging determine optimal point treatment. Finally, membrane potential depolarization, impaired function, activation caspase-3, ultimately amplification apoptosis.
Language: Английский
Citations
0