Antioxidants in cancer therapy mitigating lipid peroxidation without compromising treatment through nanotechnology DOI Creative Commons
Daniel Ejim Uti, Item Justin Atangwho, Esther Ugo Alum

et al.

Discover Nano, Journal Year: 2025, Volume and Issue: 20(1)

Published: April 24, 2025

Cancer treatments often exploit oxidative stress to selectively kill tumour cells by disrupting their lipid peroxidation membranes and inhibiting antioxidant enzymes. However, plays a dual role in cancer progression, acting as both promoter suppressor. Balancing through therapy remains challenge, excessive activity may compromise the efficacy of chemotherapy radiotherapy. This review explores antioxidants mitigating while maintaining treatment efficacy. It highlights recent advancements nanotechnology-based targeted delivery optimize therapeutic outcomes. A comprehensive literature was conducted using reputable databases, including PubMed, Scopus, Web Science, ScienceDirect. The search focused on publications from past five years (2020-2025), supplemented relevant studies earlier years. Keywords such "antioxidants," "lipid peroxidation," "nanotechnology therapy," "oxidative stress" were utilized. Relevant articles critically analysed, graphical illustrations created. Emerging evidence suggests that nanoparticles, liposomes, polymeric metal-organic frameworks, others, can effectively encapsulate control release minimizing systemic toxicity. Stimuli-responsive carriers with tumour-specific targeting mechanisms further enhance delivery. Studies indicate these strategies help preserve normal cells, mitigate stress-related damage, improve challenges bioavailability, stability, potential interactions standard therapies remain. Integrating nanotechnology antioxidant-based interventions presents promising approach for optimizing therapy. Future research should focus refining modulation strategies, assessing profiles during treatment, employing biomarkers determine optimal dosing. balanced use adverse effects.

Language: Английский

Mechanisms of ferroptosis in Alzheimer's disease and therapeutic effects of natural plant products: A review DOI Open Access
Zhao Da, Kailin Yang, Hua Guo

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2023, Volume and Issue: 164, P. 114312 - 114312

Published: May 19, 2023

Neurodegenerative diseases, such as Alzheimer's disease (AD), are characterized by massive loss of specific neurons. It is a progressive disabling, severe and fatal complex disease. Due to its pathogenesis limitations clinical treatment strategies, it poses serious medical challenge burden worldwide. The AD not clear, potential biological mechanisms include aggregation soluble amyloid form insoluble plaques, abnormal phosphorylation tau protein formation intracellular neurofibrillary tangles (NFT), neuroinflammation, ferroptosis, oxidative stress metal ion disorders. Among them, ferroptosis newly discovered programmed cell death induced iron-dependent lipid peroxidation reactive oxygen species. Recent studies have shown that closely related AD, but the mechanism remains unclear. may be iron metabolism, amino acid metabolism affecting accumulation ions. Some chelating agents (deferoxamine, deferiprone), chloroiodohydroxyquine derivatives, antioxidants (vitamin E, lipoic acid, selenium), derivatives Fer-1, tet, etc. been in animal effective exert neuroprotective effects. This review summarizes regulation natural plant products on order provide reference information for future research development inhibitors.

Language: Английский

Citations

48
Low-dose Olaparib improves septic cardiac function by reducing ferroptosis via accelerated mitophagy flux DOI Creative Commons
Ruixue Liu, Fengjuan Li, Shuai Hao

et al.

Pharmacological Research, Journal Year: 2024, Volume and Issue: 200, P. 107056 - 107056

Published: Jan. 15, 2024

Sepsis is a dysregulated response to infection that can result in life-threatening organ failure, and septic cardiomyopathy serious complication involving ferroptosis. Olaparib, classic targeted drug used oncology, has demonstrated potential protective effects against sepsis. However, the exact mechanisms underlying its action remain be elucidated. In our study, we meticulously screened ferroptosis genes associated with sepsis, conducted comprehensive functional enrichment analyses delineate relationship between mitochondrial damage. Eight sepsis-characterized were identified sepsis patients, including DPP4, LPIN1, PGD, HP, MAPK14, POR, GCLM, SLC38A1, which significantly correlated quality imbalance. Utilizing DrugBank molecular docking, robust interaction of Olaparib these genes. Lipopolysaccharide (LPS)-stimulated HL-1 cells monocytes establish an vitro model. Additionally, vivo model was developed using mice subjected cecal ligation perforation (CLP). Intriguingly, low-dose (5 mg/kg) effectively mitigated markers ferroptosis, concurrently improving quality. This led marked enhancement cardiac function significant increase survival rates (p < 0.05). The mechanism through ameliorates leukocyte post-sepsis attributed facilitation mitophagy, thus favoring integrity. conclusion, findings suggest improve by accelerating mitophagy flux, consequently inhibiting preserving after

Language: Английский

Citations

18
Tumor microenvironment triggered iron-based metal organic frameworks for magnetic resonance imaging and photodynamic-enhanced ferroptosis therapy DOI
Manman Xie,

Canran Jiang,

Cong Zhang

et al.

Journal of Colloid and Interface Science, Journal Year: 2025, Volume and Issue: 685, P. 382 - 395

Published: Jan. 17, 2025

Language: Английский

Citations

3
Combined photothermal and photodynamic therapy enhances ferroptosis to prevent cancer recurrence after surgery using nanoparticle-hydrogel composite DOI
Lu Chen, Gaojie Chen,

Kang Hu

et al.

Chemical Engineering Journal, Journal Year: 2023, Volume and Issue: 468, P. 143685 - 143685

Published: May 22, 2023

Language: Английский

Citations

31
Ferroptosis: the emerging player in remodeling triple-negative breast cancer DOI Creative Commons
Jie Li, Dejiao He, Sicheng Li

et al.

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: Oct. 20, 2023

Triple-negative breast cancer (TNBC) is a highly heterogeneous tumor type that malignant, invasive, and recurrent. Ferroptosis unique mode of programmed cell death (PCD) at the morphological, physiological, molecular levels, mainly characterized by induced iron-dependent accumulation lipid peroxides, which plays substantial role in variety diseases, including tumors inflammatory diseases. TNBC cells have been reported to display peculiar equilibrium metabolic profile iron glutathione, may increase sensitivity ferroptosis. possesses higher ferroptosis than other types. also occurred between immune cells, suggesting regulating remodel modulating response. Many ferroptosis-related genes or molecules characteristic expression patterns are expected be diagnostic targets for TNBC. Besides, therapeutic strategies based on ferroptosis, isolation extraction natural drugs use inducers, urgent personalized treatment. Thus, this review will explore contribution progression, diagnosis, treatment, provide novel perspectives management.

Language: Английский

Citations

29
Mitochondrial GPX4 acetylation is involved in cadmium-induced renal cell ferroptosis DOI Creative Commons

Yue‐Yue Guo,

Nannan Liang,

Xiaoyi Zhang

et al.

Redox Biology, Journal Year: 2024, Volume and Issue: 73, P. 103179 - 103179

Published: May 8, 2024

Increasing evidences demonstrate that environmental stressors are important inducers of acute kidney injury (AKI). This study aimed to investigate the impact exposure Cd, an stressor, on renal cell ferroptosis. Transcriptomics analyses showed arachidonic acid (ARA) metabolic pathway was disrupted in Cd-exposed mouse kidneys. Targeted metabolomics oxidized ARA metabolites were increased mice. Renal 4-HNE, MDA, and ACSL4, upregulated Consistent with animal experiments, vitro experiments mitochondrial lipids elevated HK-2 cells. Ultrastructure membrane rupture Mitochondrial cristae accordingly reduced SIRT3, NAD

Language: Английский

Citations

15
Co-exposure of arsenic and polystyrene-nanoplastics induced kidney injury by disrupting mitochondrial homeostasis and mtROS-mediated ferritinophagy and ferroptosis DOI

Gaolong Zhong,

Baoxin Qiao,

Ying He

et al.

Pesticide Biochemistry and Physiology, Journal Year: 2024, Volume and Issue: 201, P. 105904 - 105904

Published: April 10, 2024

Language: Английский

Citations

10
Sirt6 overexpression relieves ferroptosis and delays the progression of diabetic nephropathy via Nrf2/GPX4 pathway DOI Creative Commons

Lingyu Du,

Canghui Guo,

Shengnan Zeng

et al.

Renal Failure, Journal Year: 2024, Volume and Issue: 46(2)

Published: July 31, 2024

Objective Sirt6, reactive oxygen species and ferroptosis may participate in the pathogenesis of Diabetic Nephropathy (DN). Exploring relationship between oxidative stress, provides new scientific ideas to DN.

Language: Английский

Citations

10
Ferroptosis: an important player in the inflammatory response in diabetic nephropathy DOI Creative Commons
Jialing Li, Luxin Li, Zhen Zhang

et al.

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: Dec. 4, 2023

Diabetic nephropathy (DN) is a chronic inflammatory disease that affects millions of diabetic patients worldwide. The key to treating DN early diagnosis and prevention. Once the patient enters clinical proteinuria stage, renal damage difficult reverse. Therefore, developing treatment methods critical. pathogenesis results from various factors, among which immune response inflammation play major roles. Ferroptosis newly discovered type programmed cell death characterized by iron-dependent lipid peroxidation excessive ROS production. Recent studies have demonstrated activation closely related occurrence development ferroptosis. Moreover, hyperglycemia induces iron overload, peroxidation, oxidative stress, inflammation, fibrosis, all are pathogenesis, indicating ferroptosis plays role in DN. this review focuses on regulatory mechanisms ferroptosis, mutual processes involved inflammation. By discussing analyzing relationship between DN, we can deepen our understanding develop new therapeutics targeting or inflammation-related for with

Language: Английский

Citations

22
Molecular regulation and therapeutic implications of cell death in pulmonary hypertension DOI Creative Commons
Enze Wang,

Sijing Zhou,

Daxiong Zeng

et al.

Cell Death Discovery, Journal Year: 2023, Volume and Issue: 9(1)

Published: July 12, 2023

Abstract Pulmonary hypertension (PH) is a clinical and pathophysiological syndrome caused by changes in pulmonary vascular structure or function that results increased resistance arterial pressure, it characterized endothelial dysfunction, artery media thickening, remodeling, right ventricular hypertrophy, all of which are driven an imbalance between the growth death cells. Programmed cell (PCD), different from necrosis, active cellular mechanism activated response to both internal external factors precisely regulated More than dozen PCD modes have been identified, among apoptosis, autophagy, pyroptosis, ferroptosis, necroptosis, cuproptosis proven be involved pathophysiology PH varying degrees. This article provides summary regulatory patterns their potential effects on PH. Additionally, describes current understanding this complex interconnected process analyzes therapeutic targeting specific as molecular targets.

Language: Английский

Citations

18