With the threat posed by drug-resistant pathogenic bacteria, developing non-antibiotic strategies for eradicating clinically prevalent superbugs remains challenging. Ferroptosis is a newly discovered form of regulated cell death that can overcome drug resistance. Emerging evidence shows the potential of triggering ferroptosis-like for antibacterial therapy, but the direct delivery of iron species is inefficient and may cause detrimental effects. Herein, an effective strategy to induce bacterial nonferrous ferroptosis-like by coordinating single-atom metal sites (e.g., Ir and Ru) into the sp2 -carbon-linked covalent organic framework (sp2 c-COF-Ir-ppy2 and sp2 c-COF-Ru-bpy2 ) is reported. Upon activating by light irradiation or hydrogen peroxide, the as-constructed Ir and Ru single-atom catalysts (SACs) can significantly expedite intracellular reactive oxygen species burst, enhance glutathione depletion-related glutathione peroxidase 4 deactivation, and disturb the nitrogen and respiratory metabolisms, leading to lipid peroxidation-driven ferroptotic damage. Both SAC inducers show potent antibacterial activity against Gram-positive bacteria, Gram-negative bacteria, clinically isolated methicillin-resistant Staphylococcus aureus (MRSA), and biofilms, as well as excellent biocompatibility and strong therapeutic and preventive potential in MRSA-infected wounds and abscesses. This delicate nonferrous ferroptosis-like strategy may open up new insights into the therapy of drug-resistant pathogen infection.

Cyanobacteria are globally widespread photosynthetic prokaryotes and are major contributors to global biogeochemical cycles. One of the most critical processes determining cyanobacterial eco-physiology is cellular death. Evidence supports the existence of controlled cellular demise in cyanobacteria, and various forms of cell death have been described as a response to biotic and abiotic stresses. However, cell death research in this phylogenetic group is a relatively young field and understanding of the underlying mechanisms and molecular machinery underpinning this fundamental process remains largely elusive. Furthermore, no systematic classification of modes of cell death has yet been established for cyanobacteria. In this work, we analyzed the state of knowledge in the field of cyanobacterial cell death. Based on that, we propose unified criterion for the definition of accidental, regulated, and programmed forms of cell death in cyanobacteria based on molecular, biochemical, and morphologic aspects following the directions of the Nomenclature Committee on Cell Death (NCCD). With this, we aim to provide a guide to standardize the nomenclature related to this topic in a precise and consistent manner, which will facilitate further ecological, evolutionary, and applied research in the field of cyanobacterial cell death.