Antifungal Drug Resistance: Molecular Mechanisms in Candida albicans and Beyond

Lee, Yunjin; Puumala, Emily; Robbins, Nicole; Cowen, Leah E.

doi:10.1021/acs.chemrev.0c00199

Cited by 823Antifungal resistance and susceptibilityFungal Plant Pathogen ControlFungal and yeast genetics research

Antifungal Drug Resistance: Molecular Mechanisms in Candida albicans and Beyond

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Lee, Yunjin, Puumala, Emily, Robbins, Nicole, Cowen, Leah E.·2021·Chemical Reviews

DOI 10.1021/acs.chemrev.0c00199PMC PMC8519031

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Abstract

Fungal infections are a major contributor to infectious disease-related deaths across the globe. Candida species are among the most common causes of invasive mycotic disease, with Candida albicans reigning as the leading cause of invasive candidiasis. Given that fungi are eukaryotes like their human host, the number of unique molecular targets that can be exploited for antifungal development remains limited. Currently, there are only three major classes of drugs approved for the treatment of invasive mycoses, and the efficacy of these agents is compromised by the development of drug resistance in pathogen populations. Notably, the emergence of additional drug-resistant species, such as Candida auris and Candida glabrata, further threatens the limited armamentarium of antifungals available to treat these serious infections. Here, we describe our current arsenal of antifungals and elaborate on the resistance mechanisms Candida species possess that render them recalcitrant to therapeutic intervention. Finally, we highlight some of the most promising therapeutic strategies that may help combat antifungal resistance, including combination therapy, targeting fungal-virulence traits, and modulating host immunity. Overall, a thorough understanding of the mechanistic principles governing antifungal drug resistance is fundamental for the development of novel therapeutics to combat current and emerging fungal threats.

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Large-scale genomic alterations, including aneuploidy, loss-of-heterozygosity, and chromosomal rearrangements, can affect the expression of drug targets, efflux pumps, and other resistance factors.
“In addition, large-scale genomic alterations, including aneuploidy, loss-of-heterozygosity (LOH), and chromosomal rearrangements, can affect the expression of drug targets, efflux pumps, and other resistance factors (7).”
From Potential role of lysine acetylation in the stepwise adaptation of Candida albicans to fluconazole (2025) · cites this paper as [7]
ERG11 mutations lead to either overexpression of the enzyme itself or alterations in its activity that lower fluconazole's binding strength.
“These mutations lead to either the overexpression of the enzyme itself (14) or alterations in its activity that can lower fluconazole’s binding strength, leading to reduced drug effectiveness (15).”
From Candida albicans enhances iron uptake to maintain fluconazole resistance (2025) · cites this paper as [15]
The echinocandins display negligible antifungal activity against Cryptococcus spp.
“the only new class of antifungal drugs developed in decades, the echinocandins, displays negligible antifungal activity against Cryptococcus spp.”
From Treatment strategies for cryptococcal infection: challenges, advances and future outlook (2021) · cites this paper as [2]
Cryptococcus spp. are intrinsically resistant to echinocandins and employ defences that enable resistance to azoles.
“Treatment options for invasive cryptococcal infection are limited, given that Cryptococcus spp. are intrinsically resistant to echinocandins and that they employ an arsenal of defences that enable resistance to azoles2,8.”
From Treatment strategies for cryptococcal infection: challenges, advances and future outlook (2021) · cites this paper as [2]
Amphotericin B has been the primary treatment for cryptococcal infection for more than half a century, despite causing substantial toxicity and limited availability due to economic and logistical constraints.
“the polyene amphotericin B has been the primary treatment for cryptococcal infection for more than half a century, despite the fact that it causes substantial toxicity and that its availability is limited by economic and logistical constraints2,4”
From Treatment strategies for cryptococcal infection: challenges, advances and future outlook (2021) · cites this paper as [2]

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[128]Besterman J; Nguyen DT; Ste-Croix H MGCD290, an Oral Fungal Hos2 Inhibitor, Enhances the Antifungal Properties of Fluconazole Following Multiple-or Single-Dose Oral Administration in Pre-and Post-Infection Settings. In Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC); MethylGene, Inc.: San Francisco, CA, 2012; Vol. Poster M-1711.

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Authors: Lee, Y., Puumala, E., Robbins, N., & Cowen, L. E.
Affiliations: University of Toronto (CA)
Corresponding author: Cowen, Leah E.
ORCID: Lee, Yunjin
Puumala, Emily
Robbins, Nicole
Cowen, Leah E.
Venue: Chemical Reviews
Publisher: American Chemical Society (ACS)
Published: 2020-05-22
Volume: 121
Issue: 6
Pages: 3390-3411
ISSN: 0009-2665 (ISSN-L)
1520-6890
DOI: 10.1021/acs.chemrev.0c00199
PMC: PMC8519031
OpenAlex: W3026958586
Cited by: 801
References: 237
Citations by year: 2026: 109 · 2025: 192 · 2024: 168 · 2023: 133 · 2022: 132 · 2021: 63 · 2020: 4
FWCI: 3.96
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: doi.org/10.15223/policy-029 (stm-asf)
doi.org/10.15223/policy-037 (stm-asf)
doi.org/10.15223/policy-045 (stm-asf)
Locations: Chemical Reviews (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Canadian Institutes of Health Research (FDN-154288)
National Institute of Allergy and Infectious Diseases (1R01AI127375-01)
Topics: Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
Life Sciences › Agricultural and Biological Sciences › Ecology, Evolution, Behavior and Systematics › Fungal Plant Pathogen Control
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
Keywords: antifungal resistance, Candida albicans, Candida auris, Candida glabrata, invasive candidiasis, antifungal agents, molecular mechanisms of resistance, combination antifungal therapy, fungal virulence factors, emerging fungal pathogens
MeSH terms: Drug Development, Animals, Antifungal Agents, Candida, Candida albicans, Drug Therapy, Combination, Humans, Mycoses, Virulence, Molecular Structure, Signal Transduction, Drug Resistance, Fungal, Candida glabrata

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Antifungal Drug Resistance: Molecular Mechanisms in Candida albicans and Beyond

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