ArticleFrontiers in immunology2025
CAV1 promotes epithelial-to-mesenchymal transition (EMT) and chronic renal allograft interstitial fibrosis by activating the ferroptosis pathway.
Article in Frontiers in immunology, 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
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
5 citing papers in PubMed.
- Syringaresinol alleviates acetaminophen-induced hepatocyte ferroptosis through the Nrf2/HO-1 pathway by targeting Caveolin-1.Chinese medicine · 2026Article
- Polyethylene terephthalate microplastics impair erectile function through macrophage mediated cGAS-STING ferroptosis.iScience · 2026Article
- Mendelian Randomization and ScTranscriptomics Reveal a Lipid Low Malignant Cells Driving Immunosuppression and Matrix Remodeling in Oral squamous cell carcinoma.International dental journal · 2026Article
- Renal allograft interstitial fibrosis: multicellular interactions and therapeutic strategies.Frontiers in immunology · 2026Review
- The contribution of ferroptosis to the epithelial-mesenchymal transition phenotype in models of age-related macular degeneration.Frontiers in cell and developmental biology · 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
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Chronic allograft dysfunction (CAD) stands as a critical factor that limits the long-term viability of transplanted kidneys. Ferroptosis is an iron-dependent form of programmed cell death increasingly linked to chronic fibrosis. However, the mechanism by which ferroptosis contributes to the onset and progression of CAD remains unclear. Methods: This study analyzed transcriptome data from renal transplant biopsy samples in the Gene Expression Omnibus (GEO), through clinical samples, animal models, and cell experiments, this study investigated the mechanism by which Caveolin-1 (CAV1) promotes CAD through the regulation of the ferroptosis pathway. Results: The elevated levels of CAV1 were found to positively correlate with CAD incidence. Clinical and animal model validation confirmed heightened CAV1 expression in CAD. Conclusion: CAV1 plays a critical role in the development of CAD by promoting EMT and chronic renal allograft interstitial fibrosis through the ferroptosis pathway. Adjusting ferroptosis by altering the expression abundance of CAV1 may become an important method for the prevention and treatment of CAD in the future.
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.