Evidence map›Paper›PMID 34958354›Full record

ReviewFEMS yeast research2022

What 'Omics can tell us about antifungal adaptation.

Gabriela Fior Ribeiro, Eszter Denes, Helen Heaney, Delma S Childers

Abstract readReview
In one paragraph

Review in FEMS yeast research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Article
  3. The proteomic response ofmicroLife · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Gabriela Fior RibeiroUniversity of Aberdeen, Institute of Medical Sciences, Aberdeen Fungal Group, Aberdeen, UK, AB25 2ZD.
Eszter DenesUniversity of Aberdeen, Institute of Medical Sciences, Aberdeen Fungal Group, Aberdeen, UK, AB25 2ZD.
Helen HeaneyUniversity of Aberdeen, Institute of Medical Sciences, Aberdeen Fungal Group, Aberdeen, UK, AB25 2ZD.
Delma S ChildersUniversity of Aberdeen, Institute of Medical Sciences, Aberdeen Fungal Group, Aberdeen, UK, AB25 2ZD.ORCID 0000-0003-2869-7332

Funding

Academy of Medical Sciences SBF006\1128BBSRCUniversity of Aberdeen
6 · The paper itself

Abstract

Invasive candidiasis, the most frequent healthcare-associated invasive fungal infection, is commonly caused by Candida albicans. However, in recent years other antifungal-resistant Candida species-namely Candida glabrata and Candidaauris-have emerged as a serious matter of concern. Much of our understanding of the mechanisms regulating antifungal resistance and tolerance relies on studies utilizing C. albicans, C. glabrataand the model yeast Saccharomyces cerevisiae. 'Omics studies have been used to describe alterations in metabolic, genomic and transcriptomic expression profiles upon antifungal treatment of fungal cells. The physiological changes identified by these approaches could significantly affect fungal fitness in the host and survival during antifungal challenge, as well as provide further understanding of clinical resistance. Thus, this review aims to comparatively address 'omics data for C. albicans, C. glabrata andS. cerevisiae published from 2000 to 2021 to identify what these technologies can tell us regarding cellular responses to antifungal therapy. We will also highlight possible effects on pathogen survival and identify future avenues for antifungal research.

Indexed as

Antifungal AgentsCandidiasisCandida albicansCandida glabrataDrug Resistance, FungalHumansMicrobial Sensitivity TestsAntifungal AgentsantifungalsCandida albicansCandida glabrata'OmicsresistanceSaccharomyces cerevisiae

Identifiers

PMID34958354
PMCPMC8755904

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.