ArticleCellular & molecular biology letters2026
SLC25A11-mediated reprogramming of mitochondrial redox state and lipid peroxidation confers NRF2-dependent ferroptosis resistance in biliary tract cancer.
Article in Cellular & molecular biology letters, 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.
- SLC25 in intestinal inflammation: mechanisms, pathological roles, and therapeutic implications.Frontiers in immunology · 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
12 authors.
Funding
Abstract
backgroundBiliary tract cancer is a group of highly heterogeneous and metastatic malignancies of the biliary tract. Current clinical treatment strategies and diagnostic methods need further improvement to effectively manage this disease.
methodsWe performed multiomics integrative and in silico analyses of selected SLC25 family members. Cell models with SLC25A11 overexpression or knockdown can be used for various biological function assays and cell imaging. Animal models and clinical specimens can be used to evaluate prognosis and treatment.
resultsSLC25A11 inhibition significantly reduced cell migration and proliferation both in vitro and in vivo. In addition, loss of SLC25A11 leads to accumulation of TCA-related metabolites, alters mitochondrial homeostasis, and reduces mitochondrial membrane potential. In addition, we confirmed that lipid peroxidation and lipid ROS aggregation in mitochondria by SLC25A11-knockdown model. Based on our RNA sequencing data, inhibition of SLC25A11 reduces NRF2 expression and translocation, resulting in loss of interaction affinity with the ferroptosis suppressor FSP1 and subsequent reactivation of the ferroptosis machinery. We also showed that low levels of SLC25A11 and knockdown models can activate lipid peroxidation and related molecules ACSL4, LPCAT3, and PEBP1, further inducing ferroptosis. Furthermore, recruitment of ferrostatin-1 (Fer-1) antagonizes the ferroptosis state by reducing lipid peroxidation and blocking the expression levels of these related molecules.
conclusionsBringing all the evidence together, we added several important insights between ferroptosis and biliary tract cancer. We raised that SLC25A11 will serve as a novel prognostic factor and treatment strategy for biliary tract cancer.
Indexed as
Identifiers
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.