ArticleAllergy2025
Targeting the Galectin-7/TRPM2/Zn
Article in Allergy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- New Insights Into Immunomodulatory Strategies for Drug Hypersensitivity Reactions: An EAACI Task Force Report.Clinical and translational allergy · 2026Review
- Astragalus polysaccharide promotes latent HIV-1 reactivation via exosome-mediated modulation of the PI3K/AKT/NF-κB axis.Extracellular vesicles and circulating nucleic acids · 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
17 authors.
Funding
Abstract
backgroundStevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) represent a spectrum of severe drug-induced cutaneous reactions. These conditions are characterized by widespread and confluent keratinocyte apoptosis, which differentiates them from erythema multiforme (EM). Mounting evidence has implicated the mitochondrial-dependent apoptosis pathway in the pathogenesis of SJS/TEN, but the potential roles and specific mechanisms of these pathways in SJS/TEN remain largely unexplored.
methodsProteomic analyses were conducted to investigate differential protein expression in blister fluid (BF)-derived exosomes from suction surgery in healthy individuals (Con Exo) or patients with EM (EM Exo) or SJS/TEN (TEN Exo). Further analysis involved glutathione S-transferase (GST) pull-down assay, liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis, and validation of MS results through proximity ligation assay (PLA) and coimmunoprecipitation (co-IP). Phenotypic and mechanistic analyses were performed using immunohistochemistry (IHC) staining, enzyme-linked immunosorbent assay (ELISA), western blotting, reverse transcription-polymerase chain reaction (RT-PCR), co-IP, CCK-8 assay, adenosine triphosphate (ATP) level measurements, and flow cytometry.
resultsGalectin-7 was markedly upregulated in BF-derived exosomes from SJS/TEN patients and showed a correlation with disease severity. Further analysis confirmed the interaction between galectin-7 and transient receptor potential (melastatin) 2 (TRPM2). BF-derived exosomes from SJS/TEN patients induced an imbalance in mitochondrial dynamics via galectin-7/TRPM2 upregulation. Activation of TRPM2 led to an elevation in mitochondrial Zn
conclusionsTargeting the galectin-7/TRPM2/Zn
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.