ReviewInternational journal of microbiology2013
Novel Regulatory Mechanisms of Pathogenicity and Virulence to Combat MDR in Candida albicans.
Review in International journal of microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed.
- Sodium lignosulfonate inhibits multiple virulent proteins of human fungal pathogen Candida albicans.Archives of microbiology · 2024Article
- Heterologous expression of the insect SVWC peptide WHIS1 inhibitsFrontiers in microbiology · 2024Article
- Molecular dissection studies ofFrontiers in microbiology · 2023Article
- A novel anti Candida albicans drug screening system based on high-throughput microfluidic chips.Scientific reports · 2019Article
- Hyporientalin A, an anti-Candida peptaibol from a marine Trichoderma orientale.World journal of microbiology & biotechnology · 2018Article
- Fungicidal action of geraniol against Candida albicans is potentiated by abrogated CaCdr1p drug efflux and fluconazole synergism.PloS one · 2018Article
- microRNAs Involved in the Control of Innate Immunity in Candida Infected Caenorhabditis elegans.Scientific reports · 2016Article
- Anticandidal Effect and Mechanisms of Monoterpenoid, Perillyl Alcohol against Candida albicans.PloS one · 2016Article
- Iron Deprivation Affects Drug Susceptibilities of Mycobacteria Targeting Membrane Integrity.Journal of pathogens · 2015Article
- Iron Acquisition Mechanisms: Promising Target Against Mycobacterium tuberculosis.The open microbiology journal · 2015Article
- Therapeutic Potential of Dietary Phenolic Acids.Advances in pharmacological sciences · 2015Review
- Advances in targeting the vacuolar proton-translocating ATPase (V-ATPase) for anti-fungal therapy.Frontiers in pharmacology · 2014Review
- Sesamol: a natural phenolic compound with promising anticandidal potential.Journal of pathogens · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Continuous deployment of antifungals in treating infections caused by dimorphic opportunistic pathogen Candida albicans has led to the emergence of drug resistance resulting in cross-resistance to many unrelated drugs, a phenomenon termed multidrug resistance (MDR). Despite the current understanding of major factors which contribute to MDR mechanisms, there are many lines of evidence suggesting that it is a complex interplay of multiple factors which may be contributed by still unknown mechanisms. Coincidentally with the increased usage of antifungal drugs, the number of reports for antifungal drug resistance has also increased which further highlights the need for understanding novel molecular mechanisms which can be explored to combat MDR, namely, ROS, iron, hypoxia, lipids, morphogenesis, and transcriptional and signaling networks. Considering the worrying evolution of MDR and significance of C. albicans being the most prevalent human fungal pathogen, this review summarizes these new regulatory mechanisms which could be exploited to prevent MDR development in C. albicans as established from recent studies.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.