ReviewFEMS yeast research2025
Antifungal drug resistance in Candida glabrata: role of cellular signaling and gene regulatory networks.
Review in FEMS yeast research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Building a Global Innovation Pipeline for Organometallic Antifungals Against Nakaseomyces glabratus: Correspondence on Maqueda-Cabrera and Cuéllar-Cruz.Current microbiology · 2026Article
- Alkylamidobetaines Induced Changes in Multidrug-Resistant, BiofilmingInternational journal of molecular sciences · 2026Article
- Mucoadhesive Gel Based onPharmaceutics · 2026Article
- Recent Outbreaks, Resistance Trends, and Control Measures inJournal of fungi (Basel, Switzerland) · 2026Review
- Review
- Not all "Candida" are "Candida": Nakaseomyces glabratus (H.W. Anderson) Sugita & M. Takask. 2022 onychomycosis and the need for rapid diagnostic.FEMS microbiology letters · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Nakaseomyces glabratus (Candida glabrata) is an opportunistic human fungal pathogen of high priority that shares an ancestor with the non-pathogenic yeast Saccharomyces cerevisiae. Candida glabrata causes infections of the mucosal surfaces as well as fatal deep-seated tissue infections in immunocompromised individuals. The co-resistance to two commonly used antifungal drug classes, azoles and echinocandins, is increasingly being reported in clinical isolates of C. glabrata all over the world, which poses a significant threat to the successful treatment of C. glabrata infections. Acquisition of drug resistance in hospital settings is a complex multifaceted process that is governed by various factors including antimicrobial stewardship. This review summarizes both the key clinical antifungal resistance mechanisms, and the contribution of cellular stress signaling pathways to drug resistance acquisition in C. glabrata. Specifically, we discuss the emerging concepts regarding the role of mitochondrial functions, epigenetic modifications, and the host niche in the development of drug resistance. Lastly, we outline some potential areas for future research that will enable us to better understand the drug evolutionary dynamics of this important human fungal pathogen.
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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.