Advances in experimental medicine and biology, Journal Year: 2024, Volume and Issue: unknown, P. 373 - 390
Published: Jan. 1, 2024
Language: Английский
Advances in experimental medicine and biology, Journal Year: 2024, Volume and Issue: unknown, P. 373 - 390
Published: Jan. 1, 2024
Language: Английский
Nature Reviews Molecular Cell Biology, Journal Year: 2024, Volume and Issue: 25(6), P. 424 - 442
Published: Feb. 16, 2024
Language: Английский
Citations
294Journal of Hematology & Oncology, Journal Year: 2023, Volume and Issue: 16(1)
Published: Sept. 12, 2023
Abstract Lipid metabolic reprogramming is an emerging hallmark of cancer. In order to sustain uncontrolled proliferation and survive in unfavorable environments that lack oxygen nutrients, tumor cells undergo transformations exploit various ways acquiring lipid increasing oxidation. addition, stromal immune the microenvironment also reprogramming, which further affects functional phenotypes responses. Given metabolism plays a critical role supporting cancer progression remodeling microenvironment, targeting pathway could provide novel approach treatment. This review seeks to: (1) clarify overall landscape mechanisms cancer, (2) summarize landscapes within their roles progression, (3) potential therapeutic targets for metabolism, highlight combining such approaches with other anti-tumor therapies new opportunities patients.
Language: Английский
Citations
140Nature Cell Biology, Journal Year: 2024, Volume and Issue: 26(3), P. 331 - 345
Published: March 1, 2024
Language: Английский
Citations
85Redox Biology, Journal Year: 2024, Volume and Issue: 75, P. 103211 - 103211
Published: May 30, 2024
Ferroptosis is a pervasive non-apoptotic form of cell death highly relevant in various degenerative diseases and malignancies. The hallmark ferroptosis uncontrolled overwhelming peroxidation polyunsaturated fatty acids contained membrane phospholipids, which eventually leads to rupture the plasma membrane. unique that it essentially spontaneous, uncatalyzed chemical process based on perturbed iron redox homeostasis contributing process, but nonetheless modulated by many metabolic nodes impinge cells' susceptibility ferroptosis. Among affecting sensitivity, several have emerged as promising candidates for pharmacological intervention, rendering ferroptosis-related proteins attractive targets treatment numerous currently incurable diseases. Herein, current members Germany-wide research consortium focusing research, well key external experts who made seminal contributions this rapidly growing exciting field gathered provide comprehensive, state-of-the-art review Specific topics include: basic mechanisms, vivo relevance, specialized methodologies, tools, potential contribution disease etiopathology progression. We hope article will not only established scientists newcomers with an overview multiple facets ferroptosis, also encourage additional efforts characterize further molecular pathways modulating ultimate goal develop novel pharmacotherapies tackle associated - or caused
Language: Английский
Citations
75Cell Metabolism, Journal Year: 2024, Volume and Issue: 36(6), P. 1351 - 1370.e8
Published: April 23, 2024
Language: Английский
Citations
36EMBO Molecular Medicine, Journal Year: 2024, Volume and Issue: 16(7), P. 1533 - 1559
Published: June 26, 2024
Language: Английский
Citations
19FEBS Letters, Journal Year: 2024, Volume and Issue: 598(10), P. 1207 - 1214
Published: Jan. 28, 2024
Lipid droplets (LDs) are fat storage organelles that conserved from bacteria to humans. LDs broken down supply cells with fatty acids (FAs) can be used as an energy source or membrane synthesis. An overload of FAs disrupts cellular functions and causes lipotoxicity. Thus, by acting hubs for storing excess fat, prevent lipotoxicity preserve homeostasis. LD synthesis turnover have precisely regulated maintain a balanced lipid distribution allow adaptation during stress. Here, we discuss how prolonged exposure lipids affects functions, the roles in buffering stress focusing on
Language: Английский
Citations
17Neuroscience, Journal Year: 2024, Volume and Issue: 549, P. 13 - 23
Published: May 6, 2024
Language: Английский
Citations
17International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(2), P. 788 - 788
Published: Jan. 18, 2025
Diets rich in carbohydrate and saturated fat contents, when combined with a sedentary lifestyle, contribute to the development of obesity metabolic syndrome (MetS), which subsequently increase palmitic acid (PA) levels. At high concentrations, PA induces lipotoxicity through several mechanisms involving endoplasmic reticulum (ER) stress, mitochondrial dysfunction, inflammation cell death. Nevertheless, there are endogenous strategies mitigate PA-induced its unsaturation elongation channeling storage lipid droplets (LDs), plays crucial role sequestering oxidized lipids, thereby reducing oxidative damage membranes. While extended exposure promotes reactive oxygen species (ROS) generation leading damage, acute ß-cells increases glucose-stimulated insulin secretion (GSIS), activation free fatty receptors (FFARs). Subsequently, FFARs by exogenous agonists has been suggested as potential therapeutic strategy prevent ß cells. Moreover, some acids, including oleic acid, can counteract negative impact on cellular health, suggesting complex interaction between different dietary fats outcomes. Therefore, challenge is peroxidation unsaturated acids utilization natural antioxidants. This complexity indicates necessity for further research into function diverse pathological conditions find main target against lipotoxicity. The aim this review is, therefore, examine recent data regarding mechanism underlying order identify that promote protection lipotoxicity, dysfunction apoptosis MetS obesity.
Language: Английский
Citations
3Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15
Published: Aug. 13, 2024
Glioblastoma-derived exosomes (GDEs), containing nucleic acids, proteins, fatty acids and other substances, perform multiple important functions in glioblastoma microenvironment. Tumor-derived serve as carriers of induce a shift metabolism towards oxidative phosphorylation, thus driving immune dysfunction dendritic cells (DCs). Lipid peroxidation is an characteristic ferroptosis. Nevertheless, it remains unclear whether GDEs can lipid accumulation oxidation to trigger ferroptosis DCs. In our study, we investigate the impact on DCs by inhibiting secretion through knocking down expression Rab27a using rat orthotopic model. The results show that reduce infiltrating brain decrease mature (mDCs) levels, thereby suppressing growth. Mechanistically, employed vitro treatments bone marrow-derived (BMDCs) with GDEs. indicate viability mDCs compared immature (imDCs) via NRF2/GPX4 pathway. Overall, these findings provide new insights into development immune-suppressive microenvironment interaction
Language: Английский
Citations
12