ArticleFrontiers in public health2023
SiNPs induce ferroptosis in HUVECs through p38 inhibiting NrF2 pathway.
Article in Frontiers in public health, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Neurotoxic and neurobehavioral impacts of silica nanoparticles on brain tissue of albino rats with the potential ameliorative efficacy of liposomal curcumin.Journal of molecular histology · 2025Article
- Mechanisms underlying targeted mitochondrial therapy for programmed cardiac cell death.Frontiers in physiology · 2025Review
- Silica nanoparticles-induced cytotoxicity and genotoxicity in A549 cell lines.Scientific reports · 2024Article
- Ferroptosis contributing to cardiomyocyte injury induced by silica nanoparticles via miR-125b-2-3p/HO-1 signaling.Particle and fibre toxicology · 2024Article
- Juglone induces ferroptosis in glioblastoma cells by inhibiting the Nrf2-GPX4 axis through the phosphorylation of p38MAPK.Chinese medicine · 2024Article
- Ferroptosis in Cancer Therapy: Mechanisms, Small Molecule Inducers, and Novel Approaches.Drug design, development and therapy · 2024Review
- The Genetic and Epigenetic Toxicity of Silica Nanoparticles: An Updated Review.International journal of nanomedicine · 2024Review
- Nanomedicines Targeting Ferroptosis to Treat Stress-Related Diseases.International journal of nanomedicine · 2024Review
- Molecular therapy of cardiac ischemia-reperfusion injury based on mitochondria and ferroptosis.Journal of molecular medicine (Berlin, Germany) · 2023Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Despite of growing evidence linking silica nanoparticles (SiNPs), one of the global-top-three-produced and -used nanoparticle (NP), to human health risks, there remain many knowledge gaps over the adverse effects of SiNPs exposure on cardiovascular system and the underlying molecular mechanisms. Methods: In this study, the ferroptotic effects of SiNPs (20 nm; 0, 25, 50, and 100 μg/mL) on human umbilical vein endothelial cells (HUVECs) and the possible molecular mechanism were studied with the corresponding biochemical and molecular biology assays. Results and discussion: The results showed that at the tested concentrations, SiNPs could decrease HUVEC viability, but the deferoxamine mesylate (an iron ion chelator) might rescue this reduction of cell viability. Also, increased levels of intracellular reactive oxygen species and enhanced mRNA expression of lipid oxidation enzymes (ACSL4 and LPCAT3) with increase in lipid peroxidation (malondialdehyde), but decreased ratios of intracellular GSH/total-GSH and mitochondrial membrane potential as well as reduced enzymatic activities of anti-oxidative enzymes (CAT, SOD, and GSH-PX), were found in the SiNPs-treated HUVECs. Meanwhile, increase in p38 protein phosphorylation and decrease in NrF2 protein phosphorylation with reduced mRNA expressions of downstream anti-oxidative enzyme genes (CAT, SOD1, GSH-PX, and GPX4) was identified in the SiNPs-exposed HUVECs. These data indicated that SiNPs exposure might induce ferroptosis in HUVECs
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