ReviewAging and disease2025
SLC7A11 in Fibrosis: Molecular Mechanisms and Future Prospects.
Review in Aging and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed.
- Glutathione metabolism-linked ferroptosis in human seminoma: a spatial multi-omics mapping study.Redox biology · 2026Article
- Understanding the role of hypoxia inducible factors in liver fibrosis and future therapeutic applications.iLIVER · 2026Review
- Article
- Biological Age Should Anchor Age-Related Disease Research.Aging and disease · 2026Article
- M6A RNA modification: focusing on non-small cell lung cancer progression, therapeutic strategies and challenges.Frontiers in oncology · 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Solute carrier family 7 member 11 (SLC7A11), or xCT, is a cystine-glutamate antiporter crucial for maintaining cellular antioxidant capacity through the uptake of cystine, which is vital for glutathione synthesis. This protein plays an important role in regulating ferroptosis, an iron-dependent form of cell death. Fibrosis, a pathological condition characterized by the excessive accumulation of fibrous connective tissue, is a health challenge because it can lead to organ dysfunction and failure. Emerging evidence links SLC7A11 to the regulation of fibrosis through its involvement in ferroptosis and other mechanisms. This review aims to explore the effects of SLC7A11 on fibrotic diseases in various organs. We will delve into both ferroptosis-dependent and -independent pathways and propose therapeutic strategies that target SLC7A11 to mitigate fibrosis, emphasizing the need for cell-type-specific interventions. This review provides a foundational understanding for the development of targeted treatments involving SLC7A11 for managing fibrotic diseases.
Indexed as
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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.