ArticleRedox biology2025
Oxidative stress-induced CDO1 glutathionylation regulates cysteine metabolism and sustains redox homeostasis under ionizing radiation.
Article in Redox biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Article
- Integrative multi-omics analysis unravels the metabolic landscape and reveals serum biomarkers for early diagnosis of hyperuricemia.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- Redox regulation of cell migration via Nischarin S-glutathionylation.Free radical biology & medicine · 2026Article
- Drug loaded cerium oxide nanozymes prevent radiation-Induced cataracts via suppressing the cGAS-STING pathway.Journal of nanobiotechnology · 2025Article
- Urinary metabolites associated with the long-term risk for chronic kidney disease incidence and progression in hypertensive patients.Metabolomics : Official journal of the Metabolomic Society · 2025Article
- Redox Regulation of Cell Migration via Nischarin S-glutathionylation.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress serves as a fundamental mechanism contributing to ionizing radiation-induced damage, which has significant implications for tissue injury. Cysteine dioxygenase type 1 (CDO1) catalyzes the rate-limiting step for cysteine oxidation pathway, thereby playing a crucial role in regulating cellular cysteine availability. However, the regulation of CDO1 activity and cysteine oxidation under ionizing radiation, as well as their subsequent effects on cell viability, remains largely unexplored. In this study, we provide evidence that CDO1 activity and cysteine oxidation are inhibited following radiation exposure. Mechanistically, ionizing radiation-induced oxidative stress triggers glutathionylation of CDO1 at cysteine (C) 164, which impairs CDO1 enzymatic activity by disrupting its interaction with the substrate cysteine. Furthermore, glutathionylation at CDO1 C164 is essential for maintaining cellular redox homeostasis and supports cell viability under ionizing radiation. These findings reveal a novel mechanism through which redox modifications of CDO1 regulate cysteine metabolism and glutathione synthesis under oxidative stress, thereby underscoring its potential as a therapeutic target for addressing radiation-induced injuries.
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.