Deciphering the oxidative stress response in Candida albicans

Candida species are the leading cause of invasive fungal infections, with Candida albicans being the most common one. Consequently, the World Health Organization has included C. albicans in its fungal priority pathogens list. Following infection, phagocytes (mostly macrophages) initiate a respiratory burst, producing oxidant compounds, such as hydrogen peroxide. In response, C. albicans activates a robust oxidative stress response to catalyze the oxidant molecules produced by the immune system and counteract their oxidative effects within the cell. The oxidative stress response of C. albicans implies proteomic changes, both in abundance and in post-translational modifications, that are not fully described yet. Proteins with immediate antioxidant properties, the MAPK signaling pathways, and transcription factors are involved in the response. In this review, we discuss the role of these factors and the interactions among them in C. albicans. Many of these mechanisms act as virulence traits that favor the invasive candidiasis and can be used as potential targets for antifungal drugs. • Phagocytes use oxidative stress to destroy Candida albicans during infection. • C. albicans counteracts phagocyte attacks with a robust oxidative stress response. • HOG MAPK pathway and Cap1 are the main actors in anti-oxidative signaling. • Catalase, thioredoxin, and glutathione are the major ROS scavenging systems. • Studying the oxidative stress response may reveal new antifungal targets.