Signaling pathways governing the pathobiological features and antifungal drug resistance of Candida auris
Open accessAbstract
Candida auris is an emerging multidrug-resistant fungal pathogen that poses a significant global health threat. Since its discovery in 2009, C. auris has rapidly spread worldwide, causing severe infections with high mortality rates, particularly in healthcare settings. Its ability to persist in the environment, form biofilms, and resist multiple antifungal drugs underscores the urgent need to understand its pathogenicity mechanisms and associated signaling pathways. Such insights are crucial for elucidating its unique virulence traits and developing targeted therapeutic strategies. Current studies have identified several key pathways involved in its pathogenicity and antifungal drug resistance. The Ras/cAMP/PKA pathway regulates critical virulence factors, including thermotolerance, morphological plasticity, and biofilm formation. The mitogen-activated protein kinase (MAPK) and calcineurin pathways contribute to stress responses and antifungal drug resistance. The regulation of Ace2 and morphogenesis (RAM) pathway influences cell aggregation, while the target of rapamycin (TOR) pathway affects filamentous growth and biofilm development. However, the distinct characteristics of C. auris , such as its rapid environmental spread and clade-specific traits, warrant further investigation into additional signaling pathways. This review provides a comprehensive analysis of known signaling pathways associated with C. auris pathogenicity and antifungal drug resistance, integrating insights from other fungal pathogens. By synthesizing current knowledge and identifying research gaps, this review offers new perspectives on future research directions and potential therapeutic targets against this formidable pathogen.
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Hyperactivation of the Ras/cAMP/PKA pathway by BCY1 or PDE2 deletion attenuated the virulence during murine systemic infection by reducing the ability to thrive in nutrient-deficient conditions.
“Furthermore, hyperactivation of the Ras/cAMP/PKA pathway by BCY1 or PDE2 deletion attenuated the virulence during murine systemic infection by reducing the ability to thrive in nutrient-deficient conditions [79,80].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [80]
The section on host temperature adaptation and thermotolerance (page unavailable) says that BCY1 or PDE2 deletion hyperactivates cAMP/PKA signaling, attenuates systemic virulence, and causes severe growth defects under nutrient-starved conditions within the host. It says those defects *may* lead to reduced virulence; the claim presents that proposed explanation as an established cause. (LLM, conf=0.88)
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- Authors
- Cha, H., Won, D., & Bahn, Y.-S.
- Affiliations
- Yonsei University (KR)
- Corresponding author
- Bahn, Yong-Sun
- Venue
- mBio
- Publisher
- American Society for Microbiology
- Published
- 2025-05-14
- Volume
- 16
- Issue
- 5
- Pages
- e0247523-e0247523
- ISSN
- 2150-7511 (ISSN-L)
- PMC
- PMC12077148
- OpenAlex
- W4409147890
- Cited by
- 19
- References
- 83
- Citations by year
- 2026: 16 · 2025: 3
- FWCI
- 3.33
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- mBio (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Research Foundation of Korea (RS-2021-NR058017, RS-2021-NR056582)
- Korea Institute for Advancement of Technology (RS-2024-00418203)
- Yonsei Signature Research Cluster Program (2024-22-0165)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
- Keywords
- Candida auris, antifungal resistance, MAPK signaling, calcineurin pathway, TOR signaling, biofilm formation, virulence factors, heat tolerance, morphological plasticity, stress response, antifungal drug targets
- MeSH terms
- Candida auris, Antifungal Agents, Candidiasis, Fungal Proteins, Humans, Virulence, Signal Transduction, Gene Expression Regulation, Fungal, Biofilms, Drug Resistance, Fungal, Virulence Factors
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