ArticleCNS neuroscience & therapeutics2026
c-MAF Transcriptionally Activates Slc40a1 to Repress Ferroptosis in Sepsis-Associated Encephalopathy.
Article in CNS neuroscience & therapeutics, 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.
- PPARα: Linking Cardiac Metabolism to Therapeutic Opportunities in Cardiovascular Diseases.Cells · 2026Review
- IRF9-dependent transcriptional regulation of SLC40A1 suppresses ferroptosis in dilated cardiomyopathy.Scientific reports · 2026Article
- Hyperbaric oxygen therapy in sepsis-associated encephalopathy: pathophysiological rationale, preclinical evidence, and translational challenges.Frontiers in cellular neuroscience · 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
6 authors.
Funding
Abstract
backgroundFerroptosis, an iron-dependent programmed cell death driven by lipid peroxidation, has emerged as a potential contributor to sepsis-associated encephalopathy (SAE). However, the relationship between ferroptosis and cognitive deficits following sepsis needs to be further elucidated.
methodsTranscriptome sequencing was employed to identify solute carrier family 40 member 1 (Slc40a1) as a candidate ferroptosis-related gene in the hippocampus of septic mice. The SAE mouse model was established via cecal ligation and perforation (CLP) after treatment with recombinant adeno-associated virus 9 (AAV9)-CaMKII to knock down or overexpress musculoaponeurotic fibrosarcoma (c-Maf) or Slc40a1. We assessed cognitive performance, Nissl staining, and ferroptosis-associated parameters. Dual-luciferase reporter gene assays and chromatin immunoprecipitation assays were performed to illuminate the mechanism by which c-MAF transcriptionally activates Slc40a1.
resultsHippocampal neurons of mice subjected to CLP showed downregulation of Slc40a1. Neuron-specific knockdown of Slc40a1 or c-Maf deteriorated sepsis-induced cognitive impairment, oxidative stress, and ferroptosis. Conversely, overexpression of Slc40a1 or c-Maf attenuated acute mortality and cognitive impairment following CLP, hampered lipid peroxidation and iron deposition, and enhanced antioxidant capacity. Moreover, Slc40a1 silencing neutralized the anti-ferroptotic property of c-Maf in SAE. Mechanistically, c-MAF was found to directly bind to the Slc40a1 promoter and facilitate its transcription.
conclusionsOur findings suggest that c-MAF/Slc40a1 may represent a promising prevention target for SAE.
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.