ArticleFrontiers in microbiology2026
ROS-implicated apoptosis in
Article in Frontiers in microbiology, 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
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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.
- Sphingolipid Metabolism in Oral Diseases: Pathogenic Mechanisms, Biomarkers, and Therapeutic Opportunities.Biomedicines · 2026Review
- Regulated Cell Death in Fungi, the Role of Metacaspases and Assay Techniques.Methods and protocols · 2026Review
- Anti-Candida albicans effect of the new antifungal compound Venetin-1 obtained from earthworms versus amphotericin B.Scientific reports · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Aureobasidin A (AbA) is a natural antifungal lipopeptide known to inhibit inositol phosphorylceramide (IPC) synthase. While its antifungal effect, mechanism via the inositol pathway involved in sphingolipid synthesis, and influence on ABC efflux pumps have been reported previously, its potential role in inducing programmed cell death and efficacy against oral candidiasis remain unexplored. This study aimed to elucidate a novel, complementary mechanism of AbA against Methods: Results: AbA potently inhibited the growth and key virulence of Conclusion: Beyond its known effect on sphingolipid synthesis, AbA exerts potent antifungal effects, which our data suggest involve the induction of ROS accumulation and subsequent mitochondrial dysfunction, leading to apoptosis. This dual mechanism highlights its promise as a therapeutic candidate, especially against azole-resistant infections.
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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.