The role of Candida albicans stress response pathways in antifungal tolerance and resistance

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 Ca2+-calmodulin-activated phosphatase calcineurin, the protein kinase C cell wall interity 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.

Automated summary

Human fungal pathogens, such as Candida albicans, are causing devastating diseases worldwide, and the increasing drug resistance poses a threat to treatment options. Understanding the cellular stress response pathways involved in antifungal resistance and tolerance is crucial for developing effective treatments. This review highlights the key players and advancements in inhibiting these pathways, and their implications for host persistence of C. albicans.