Review evaluates the antibacterial mechanisms of porous silicon in combating antimicrobial resistance, suggesting new strategies.
The escalating global crisis of antimicrobial resistance (AMR) requires a deeper fundamental understanding of bactericidal strategies that operate independently of biochemical pathways. Nanostructured porous silicon (PSi) fabricated via Metal-Assisted Chemical Etching (MACE) provides a highly versatile platform to investigate these alternatives due to its tunable nanotopography. This review evaluates the multimodal antibacterial mechanisms of MACE-PSi, with a focus on its utility as a model system for elucidating topography-pathogen interactions. We detail the biophysical processes whereby high-aspect-ratio silicon architectures exert physical forces that stretch and rupture bacterial envelopes. Furthermore, we analyze the synergistic chemical effects arising from localized silicon dissolution and residual metal catalysts (e.g., Ag, Au, Pt, Cu). By critically examining physiological variables that impact these mechanisms, such as protein corona formation, biofilm dynamics, and structural stability, this review highlights both the current analytical capabilities and the practical limitations of using MACE-PSi to study mechano-bactericidal interfaces.
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Ramírez et al. (2026) studied this question.
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