ArticleInvestigative ophthalmology & visual science2025
Fusarium solani Activates PANoptosis and Modulates Immune Response in Fungal Keratitis.
Article in Investigative ophthalmology & visual science, 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.
- Role of PANoptosis in cancer: molecular mechanisms and therapeutic insights.Archives of toxicology · 2026Review
- Z-Nucleic Acids: A Regulator of Macrophage PANoptosis and Fungal Biofilm in Fungal Keratitis.Investigative ophthalmology & visual science · 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: This study aimed to investigate how Fusarium solani triggers PANoptosis in fungal keratitis and to examine the toxic impacts and underlying mechanisms of deoxynivalenol (DON) on human corneal epithelial (HCE-T) cells. Methods: A F. solani keratitis mouse model was established through intrastromal injection of fungal spores. Clinical severity was evaluated using a standardized scoring system. PANoptosis markers in corneal tissues were analyzed via western blotting, immunofluorescence, and TUNEL assay. Real-time PCR was used to quantify inflammatory cytokines. RNA sequencing was conducted to select differentially expressed genes (DEGs) and analyze immune cell infiltration profiles. HCE-T cells were exposed to DON, and PANoptosis-related proteins were detected via western blot and immunofluorescence. Gene expression alterations were analyzed using RNA sequencing. Results: PANoptosis activation was validated through upregulated expression of cleaved caspases-1, -3, -7, and -8; gasdermin D (GSDMD); and phosphorylated mixed lineage kinase domain-like protein (p-MLKL) in infected corneas, accompanied by augmented TUNEL-positive cells. Inflammatory cytokines (IL-6, IL-1β, TNF-α) were significantly upregulated. RNA sequencing revealed significant changes in PANoptosis, immune response, and extracellular matrix organization. Immune infiltration profiling indicated a marked increase in M1 macrophages in infected corneas. In vitro experiments demonstrated that DON exposure increased PANoptosis markers (cleaved caspases-1, -3, -7, and -8; BAX; GSDMD; and p-MLKL) in HCE-T cells, along with upregulation of inflammatory cytokines (IL-6, IL-1β, IL-18, TNF-α). RNA sequencing further revealed alterations in ribosomal RNA (rRNA) processing and extracellular matrix organization pathways in DON-treated cells. Conclusions: F. solani infection and DON exposure induce PANoptosis in fungal keratitis, leading to significant inflammatory responses. These results suggest that targeting PANoptosis signaling pathways may represent a novel therapeutic approach for treating fungal keratitis.
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.