ReviewMolecular medicine reports2026
Involvement of the thioredoxin system in multiple diseases: A focus on mechanisms of action in autophagy and ferroptosis (Review).
Review in Molecular medicine reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Reductive Stress and Ferroptosis: Linking Insulin Signaling to Metabolic Dysfunction.Biomolecules · 2026Review
- The Interaction Between Iron and Selenium Affects Ferroptosis in Colorectal Cancer.International journal of molecular sciences · 2026Review
- Selenium-Thioredoxin Axis Contributes to Ferroptosis Resistance in Pancreatic Cancer Cells.International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The thioredoxin (Trx) system comprises four core components: Trx‑interacting protein (TXNIP), Trx, Trx reductase (TrxR) and NADPH. TrxR utilizes NADPH to reduce Trx, reducing target proteins through its conserved thiol groups, thereby maintaining cellular redox balance. TXNIP inhibits Trx activity by forming a disulfide exchange reaction with Trx. Beyond its role in redox regulation, the Trx system interacts with various cellular regulators and participates in intracellular signaling networks. The Trx system exhibits dual regulatory roles in autophagy, with Trx primarily exerting an inhibitory effect on ferroptosis and apoptosis, whereas TXNIP promotes these processes. Multiple molecular mechanisms are implicated in these regulatory functions. Furthermore, the Trx system mediates cross‑regulation between autophagy and ferroptosis, as well as autophagy and apoptosis, thereby influencing cellular responses to stress conditions. The present review examines the structural components of the Trx system and the cellular translocation of TXNIP. Additionally, it explores the involvement of the Trx system in various diseases, including neurodegenerative disorders, cardiovascular diseases and cancer, highlighting its potential as a therapeutic target. By analyzing the molecular mechanisms through which the Trx system modulates cell death pathways, including ferroptosis, autophagy and apoptosis, the present review may provide novel research perspectives and theoretical foundations for developing disease treatment strategies.
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What 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.