The role of Candida albicans stress response pathways in antifungal tolerance and resistance
Open accessAbstract
Human fungal pathogens are the causative agents of devastating diseases across the globe, and the increasing prevalence of drug resistance threatens to undermine the already limited treatment options. One prominent pathogen is the opportunistic fungus Candida albicans , which can cause both superficial and serious systemic infections in immunocompromised individuals. C. albicans antifungal drug resistance and antifungal tolerance are supported by diverse and expansive cellular stress response pathways. Some of the major players are the Ca 2+ -calmodulin-activated phosphatase calcineurin, the protein kinase C cell wall integrity pathway, and the molecular chaperone heat shock protein 90. Beyond these core signal transducers, several other enzymes and transcription factors have been implicated in both tolerance and resistance. Here, we highlight some of the major stress response pathways, key advances in identifying chemical matter to inhibit these pathways, and implications for C. albicans persistence in the host.
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Activation of cellular stress response pathways, such as Hsp and calcineurin pathways, contributes to echinocandin tolerance in C. albicans.
“In addition, activation of cellular stress response pathways, such as the heat shock protein (Hsp) and calcineurin pathways, has been shown to contribute to echinocandin tolerance in C. albicans [120,121].”
From Insight into the Mechanisms and Clinical Relevance of Antifungal Heteroresistance (2025) · cites this paper as [121]
Hsp90 is central to stress response pathways in fungi, mediating antifungal tolerance and resistance through its interactions with key client proteins: protein phosphatase calcineurin and components of the PKC cell wall integrity pathway.
“Hsp90 is central to stress response pathways in fungi, mediating antifungal tolerance and resistance through its interactions with key client proteins: protein phosphatase calcineurin and components of the PKC cell wall integrity pathway [66,74].”
From Antifungal persistence: Clinical relevance and mechanisms (2025) · cites this paper as [66]
Stress response pathways are important for the integrity of the fungal cell wall and cell membrane and have been widely studied in antifungal tolerance and resistance.
“Stress response pathways are important for the integrity of fungal cell wall and cell membrane, thus have been widely studied in antifungal tolerance and resistance [66,67].”
From Antifungal persistence: Clinical relevance and mechanisms (2025) · cites this paper as [66]
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References 85 · Cited by 88
- Authors
- Iyer, K. R., Robbins, N., & Cowen, L. E.
- Affiliations
- University of Toronto (CA)
- Corresponding author
- Cowen, Leah E.
- Venue
- iScience
- Publisher
- Elsevier BV
- Published
- 2022-03
- Volume
- 25
- Issue
- 3
- Pages
- 103953
- ISSN
- 2589-0042 (ISSN-L)
- PMC
- PMC8905312
- OpenAlex
- W4213074258
- Cited by
- 88
- References
- 85
- Citations by year
- 2026: 12 · 2025: 26 · 2024: 24 · 2023: 19 · 2022: 7
- FWCI
- 2.00
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- iScience (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Canadian Institutes of Health Research (FDN-154288)
- Canada Research Chairs
- National Institutes of Health (R01AI120958, R01AI127375)
- Canadian Institute for Advanced Research
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
- Keywords
- Candida albicans, antifungal resistance, antifungal tolerance, stress response pathways, calcineurin, protein kinase C, cell wall integrity pathway, HSP90, transcription factors, antifungal drug targets, opportunistic fungal infection
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