ArticleApplied biochemistry and biotechnology2026
The Protective Effect of N, Ce-doped Carbon Dots Against H
Article in Applied biochemistry and biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Carbon Dots and Mitochondria-Advances in Targeting, Imaging, and Therapeutics.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Oxidative stress-induced vascular smooth muscle cell (VSMC) apoptosis plays a central role in aortic aneurysm (AA) progression. In this study, we developed N, Ce-codoped carbon dots (N, Ce-CDs, ~ 4.8 nm) as an efficient nanozyme to counteract this process. The synthesized N, Ce-CDs exhibited superior •OH radical scavenging capability and excellent biocompatibility. In vitro, N, Ce-CDs showed no cytotoxicity toward MOVAS cells, maintaining over 90% cell viability after 72 h exposure. More importantly, they demonstrated a significant protective effect against H₂O₂-induced oxidative damage. The nanozymes alleviated oxidative damage by scavenging intracellular reactive oxygen species (ROS), suppressing lipid peroxidation, and boosting endogenous antioxidant capacity through elevated levels of glutathione (GSH) and enhanced activities of superoxide dismutase (SOD) and catalase (CAT). Furthermore, N,Ce-CDs significantly mitigated H₂O₂-induced damage, recovering ~ 60% of the lost mitochondrial membrane potential (MMP) and reducing the apoptosis rate from 31.97% to 18.52%. These findings highlight the potential of N, Ce-CDs as a multifunctional nanotherapeutic agent that protects VSMCs by integrating antioxidant defense with mitochondrial stabilization, presenting a novel strategy for AA treatment.
Indexed as
Identifiers
41504846What Socratic 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 Socratic graph.