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Fungal cell processes refer to the collective biological activities required for the growth, reproduction, and survival of fungal pathogens. In a pharmacological context, this term is too broad to define a single target; instead, it encompasses several distinct molecular targets that are exploited to achieve selective toxicity against fungi while sparing human host cells [1]. Key processes targeted by current therapeutics include the synthesis of the fungal cell wall (specifically beta-1,3-D-glucan and chitin) and the maintenance of the fungal cell membrane, which relies on ergosterol rather than the cholesterol found in animal cells [2][4]. Major classes of antifungal drugs, such as azoles, polyenes, and echinocandins, work by disrupting these specific pathways to cause cell death or inhibit growth [3]. Disrupting these processes is critical for treating systemic and mucosal infections caused by species like Candida, Aspergillus, and Cryptococcus [5]. However, the similarity between some fungal and mammalian cellular machinery, such as mitochondrial functions or certain enzymes, can lead to off-target effects and clinical toxicity [4]. Sources: [1] https://www.ncbi.nlm.nih.gov/books/NBK470195/ [2] https://pmc.ncbi.nlm.nih.gov/articles/PMC4026563/ [3] https://pubmed.ncbi.nlm.nih.gov/24432131/ [4] https://www.msdmanuals.com/professional/infectious-diseases/fungi/antifungal-drugs [5] https://www.cdc.gov/fungal/infections/index.html
Interruption of fungal cell wall integrity via beta-glucan synthesis inhibition; disruption of cell membrane stability by binding to or inhibiting the synthesis of ergosterol; inhibition of fungal DNA/RNA synthesis; and interference with microtubule assembly during mitosis [1][2][3].
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