ArticleMaterials today. Bio2025
Chondroitin sulfate nanoparticles based on co-delivery dual drug induced ferroptosis in lung cancer cells by disrupting mitochondrial oxidative homeostasis.
Article in Materials today. Bio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed.
- Precision nanomedicine for pulmonary diseases: from molecular targeting to clinical translation.Signal transduction and targeted therapy · 2026Review
- A multimodal ROS generation and bimodal ferroptosis and cuproptosis self-reinforced strategy for effective bone metastases therapy.Journal of nanobiotechnology · 2026Article
- [SENP1 reduces ferroptosis of thyroid cancer cells by regulating hypoxia-inducible factor-1α].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Curcumin-mediated modulation of immunogenic cancer cell death pathways.Molecular biology reports · 2026Review
- Exploring the potential of oxymatrine in preventing CHIKV-induced acute kidney injury based on multi-dimensional computational analysis andFrontiers in microbiology · 2026Article
- Chondroitin Sulfate-Based Nanoplatforms: Advances and Challenges for Cancer Therapy.Molecules (Basel, Switzerland) · 2025Review
- Mechanism of ECM Stiffness-Integrin-Hippo-ABCG1 axis in regulating ferroptosis and targeted nanodrug intervention in LUAD.Respiratory research · 2025Article
- A biomimetic nanoplatform for multimodal imaging-guided therapy of esophageal cancer via synergistic activation of cuproptosis and ferroptosis.Materials today. Bio · 2025Article
- Curcumin-loaded nanoparticles for renal ischemia-reperfusion injuries: Triple-play of redox homeostasis accommodation, lipid metabolism regulation, and nuclear magnetic tracing.Materials today. Bio · 2025Article
- Engineered nanocarriers for targeted lung cancer therapy: mechanistic innovations and recent clinical progress.Exploration of targeted anti-tumor therapy · 2025Review
- Advances in Chondroitin Sulfate-Based Nanoplatforms for Biomedical Applications.International journal of nanomedicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial REDOX homeostasis is unbalanced by large amounts of reactive oxygen species production and reduced glutathione, leading to lipid oxidation-induced ferroptosis, which enhanced cancer immunotherapy. Thus, disrupting mitochondrial redox homeostasis represents a promising strategy for the treatment of lung cancer. In this study, a co-delivery system of based on chondroitin sulfate (CS) (CS-CA-CUR-TPP, CCCT) for natural medicines (Curcumin, CUR; and Cinnamaldehyde CA) was successfully constructed, which resulted in elevated ROS levels in cancer cells. Under the action of CS specifically targeting tumor cells, CCCT NPs is enriched and taken up by lung cancer cells. Acid responsiveness causes the CCCT NPs to break and escape from the lysosome, and CUR targets and destroys mitochondria under the action of mitochondrial target head triphenylphosphine (TPP). CA collaborates with CUR to produce large amounts of ROS and reduce GSH in a time-dependent manner in mitochondria for disruption of REDOX homeostasis, and triggers ferroptosis by reducing the expression of GXP4 and xCT proteins. The immunogenic cell death (ICD) after ferroptosis promotes interferon γ (IFN-γ), TNF-a, and IL-6 secretion. Our results desmontrat CCCT can promote inhibition of tumor growth by enhancing tumor immunogenicity. This study may provide a potential avenue for the advancement of self-delivery nanoparticles to overcome resistance to apoptosis in tumor therapy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.