ReviewThe FEBS journal2020
Targeting evolution to inhibit antibiotic resistance.
Review in The FEBS journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 44 citations in OpenAlex.
- Polymorphisms in a bacterial signalling pathway alter evolutionary routes of antibiotic resistance in Escherichia coli.PLoS biology · 2026Article
- Function-specific epistasis shapes evolutionary trajectories towards antibiotic resistance.Nature communications · 2026Article
- Benzoxaborole-Based Inhibitors Block LexA Autocleavage and Suppress SOS-Dependent Adaptive Phenotypes inAntibiotics (Basel, Switzerland) · 2026Article
- Genetic architecture of resistance to plant secondary metabolites in Photorhabdus entomopathogenic bacteria.BMC genomics · 2025Article
- Impeding pathways of intrinsic resistance in Escherichia coli confers antibiotic sensitization and resistance proofing.PLoS biology · 2025Article
- Bioenergetic stress potentiates antimicrobial resistance and persistence.Nature communications · 2025Article
- An anti-virulence drug targeting the evolvability protein Mfd protects against infections with antimicrobial resistant ESKAPE pathogens.Nature communications · 2025Article
- Snapshots ofiScience · 2025Article
- The LexA-RecA* structure reveals a cryptic lock-and-key mechanism for SOS activation.Nature structural & molecular biology · 2024Article
- Review
- A Study of the Synergistic Effects of Essential Oils fromMetabolites · 2024Article
- The global RNA-RNA interactome ofProceedings of the National Academy of Sciences of the United States of America · 2024Article
- A small molecule that inhibits the evolution of antibiotic resistance.NAR molecular medicine · 2024Article
- Review
- Investigating the composition and recruitment of the mycobacterial ImuA'-ImuB-DnaE2 mutasome.eLife · 2023Article
- Drugging evolution of antibiotic resistance at a regulatory network hub.Science advances · 2023Article
- RecA-NT homology motif in ImuB is essential for mycobacterial ImuA'-ImuB protein interaction and mutasome function.bioRxiv : the preprint server for biology · 2023Article
- Structural basis for regulation of SOS response in bacteria.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Resistance-resistant antibacterial treatment strategies.Frontiers in antibiotics · 2023Article
- Evaluation of residue variability in a conformation-specific context and during evolutionary sequence reconstruction narrows drug resistance selection in Abl1 tyrosine kinase.Protein science : a publication of the Protein Society · 2022Article
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 at 2 institutions in 1 country.
Funding
Abstract
Drug-resistant bacterial infections have led to a global health crisis. Although much effort is placed on the development of new antibiotics or variants that are less subject to existing resistance mechanisms, history shows that this strategy by itself is unlikely to solve the problem of drug resistance. Here, we discuss inhibiting evolution as a strategy that, in combination with antibiotics, may resolve the problem. Although mutagenesis is the main driver of drug resistance development, attacking the drivers of genetic diversification in pathogens has not been well explored. Bacteria possess active mechanisms that increase the rate of mutagenesis, especially at times of stress, such as during replication within eukaryotic host cells, or exposure to antibiotics. We highlight how the existence of these promutagenic proteins (evolvability factors) presents an opportunity that can be capitalized upon for the effective inhibition of drug resistance development. To help move this idea from concept to execution, we first describe a set of criteria that an 'optimal' evolvability factor would likely have to meet to be a viable therapeutic target. We then discuss the intricacies of some of the known mutagenic mechanisms and evaluate their potential as drug targets to inhibit evolution. In principle, and as suggested by recent studies, we argue that the inhibition of these and other evolvability factors should reduce resistance development. Finally, we discuss the challenges of transitioning anti-evolution drugs from the laboratory to the clinic.
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What OpenQuestion holds
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.