Introduction: Antibiotic resistance is now a serious problem for world health. Antibiotics are used excessively and frequently inappropriately in medicine, agriculture, and livestock, which has sped up the creation of resistant infections and rendered many conventional treatments useless. According to the World Health Organization, if antimicrobial resistance (AMR) is not controlled, it may result in millions of deaths every year by 2050.
Genetic factors have a major role in shaping resistance. Bacteria can neutralize, avoid, or expel medications through mutations, horizontal gene transfer, and gene control. Gaining knowledge of these processes is essential for comprehending how resistance develops and how to overcome it. In addition, nanotechnology provides creative answers. Because of their distinct physicochemical characteristics, nanoparticles (NPs) can either function directly as antimicrobial agents or enhance the effectiveness of traditional antibiotics. The main genetic pathways of bacterial resistance are highlighted in this overview, along with tactics based on nanotechnology that aim to combat it.
Methods: The scientific literature published between 2015 and 2025 was compiled in this review. Keyword combinations like bacterial resistance, genetic processes, nanoparticles, and nanotechnology were used to search databases like PubMed, Scopus, and Web of Science. The included articles addressed nanotechnology-based antimicrobial methods and genetic determinants of resistance (e.g., mutations, plasmids, efflux pumps). Excluded were studies with no mechanistic detail or those had no bearing on genetics or nanoscience. To find recurring themes and new solutions, a selection of articles were examined.
Results: Several genetic mechanisms contribute to resistance. Antibiotic targets are frequently altered by chromosomal changes. For instance, resistance to fluoroquinolones is conferred by mutations in parC or gyrA. Critical resistance genes like blaCTX-M and blaNDM, which encode β-lactamases that can break down cephalosporins and carbapenems, are distributed horizontally through plasmids and transposons. Genes such as marA and soxS are part of regulatory networks that boost efflux pump activity, which lowers intracellular antibiotic concentrations. Furthermore, reversible resistance states can be created by epigenetic processes such DNA methylation. These results collectively demonstrate that bacterial resistance is dynamic, flexible, and impacted by both regulatory and genetic variables.
Conclusion: Bacterial resistance is driven by a complex interplay of genetic mutations, horizontal gene transfer, and regulatory adaptation. These mechanisms enable rapid survival against antibiotic stress, making resistance a moving target. Nanotechnology introduces new opportunities to overcome this challenge, either by direct antimicrobial action or by enhancing current drugs. While promising, nanoparticle-based therapies must be carefully evaluated for safety, stability, and cost-effectiveness before large-scale clinical application. Integrating genetic knowledge with nanoscience could pave the way toward precision therapies that slow resistance and restore the power of antibiotics.