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Copper Single-Atoms Loaded on Molybdenum Disulphide Drive Bacterial Cuproptosis-Like Death and Interrupt Drug-Resistance Compensation Pathways

111. Wenqi Wang, Xiaolong Wei, Bolong Xu, Hengshuo Gui, Yan Yan*, Huiyu Liu* & Xianwen Wang* Nano-Micro Lett. 18,111 (2026).

This work is led by Prof. Dr. Xianwen Wang (Anhui Medical University) and co-workers. Prof. Wang’s research centers on burn wounds and tissue regeneration, burn infection, design and development of antimicrobial nanomaterials, development of anti-inflammatory nano-formulations and study on their anti-inflammatory mechanisms. This article develops copper single-atom-loaded MoS₂ nanozymes (Cu SAs/MoS₂) that combat drug-resistant bacteria through a triple mechanism of oxidative damage, cuproptosis-like death, and disrupted cell wall synthesis. Density functional theory reveals that Cu coordination enhances H₂O₂ adsorption, reducing activation energy by 17% and boosting peroxidase-like activity, while glutathione peroxidase-like activity disrupts redox homeostasis and inhibition of peptidoglycan synthesis blocks cell wall remodeling, collectively enabling efficient bacterial killing and decelerating resistance development.

Related articles: Cactus Thorn-Inspired Janus Nanofiber Membranes as a Water Diode for Light-Enhanced Diabetic Wound Healing https://doi.org/10.1007/s40820-025-01904-z Synergistic Ferroptosis–Immunotherapy Nanoplatforms: Multidimensional Engineering for Tumor Microenvironment Remodeling and Therapeutic Optimization https://doi.org/10.1007/s40820-025-01862-6 Wearable Ultrasound Devices for Therapeutic Applications https://doi.org/10.1007/s40820-025-01890-2

The development of highly efficient and multifunctional nanozymes holds promise for addressing the challenges posed by drug-resistant bacteria. Here, copper single-atom-loaded MoS2 nanozymes (Cu SAs/MoS2) were developed to effectively combat drug-resistant bacteria by synergistically integrating the triple strategies of oxidative damage, cuproptosis-like death and disruption of cell wall synthesis. Density functional theory revealed that each Cu center coordinated with three sulfur ligands, enhancing the adsorption of H2O2, which reduced the activation energy of the key step by 17%, thereby improving peroxidase-like (POD-like) activity. The generation of reactive oxygen species in combination with Cu SAs/MoS2 glutathione peroxidase-like (GSH-Px-like) for glutathione scavenging resulted in an imbalance in redox homeostasis within bacteria.

Wnt signaling drives stomach cancer spread by reshaping surrounding tissue, finds study

Researchers at the Cancer Research Institute and the Nano Life Science Institute (WPI-NanoLSI), Kanazawa University, have uncovered a critical mechanism that enables gastric cancer to spread to distant organs. Their study shows that cancer cells stimulate Wnt signaling in surrounding stromal fibroblasts to produce hyaluronan, creating a supportive microenvironment that promotes metastasis. These findings provide new insight into how metastatic tumors establish themselves and suggest promising strategies to prevent gastric cancer progression. The work is published in the journal Nature Communications.

Gastric cancer remains one of the leading causes of cancer-related deaths worldwide, largely because it frequently spreads to other organs such as the liver. While genetic mutations that initiate tumors have been extensively studied, the biological mechanisms that allow cancer cells to colonize new tissues remain poorly understood.

“Wnt signaling”—a pathway essential for stem cell maintenance and tissue regeneration—is often activated in gastric cancer through external ligand stimulation rather than genetic mutation. This study further identifies that Wnt signaling in the tumor microenvironment also plays a crucial role in disease progression.

Tubulin prevents toxic protein clumps in the brain, fighting back against neurodegeneration

Researchers at Baylor College of Medicine have discovered a potential new strategy to fight back against Alzheimer’s and Parkinson’s diseases, conditions that are linked to the toxic accumulation of Tau and alpha synuclein protein clumps in the brain. The team reports in Nature Communications that tubulin, the building block of microtubules, the cell’s internal ‘railway tracks, can stop Tau and alpha synuclein from forming toxic clumps and instead steer them into their normal, healthy roles.

“Tau and alpha synuclein are well known for their roles in neurodegenerative diseases like Alzheimer’s and Parkinson’s. In these conditions, these proteins can misfold, stick together and form harmful aggregates that damage neurons and contribute to memory loss, movement problems and other symptoms,” said first author Dr. Lathan Lucas, postdoctoral associate of biochemistry and molecular pharmacology in Dr. Allan Ferreon’s lab.

“But Tau and alpha synuclein also fulfill essential functions in healthy neurons—they help maintain cell structure and support communication by interacting with tubulin and contributing to microtubule assembly and stabilization.”

Tubulin Cytoskeleton in Neurodegenerative Diseases–not Only Primary Tubulinopathies

Neurodegenerative diseases represent a large group of disorders characterized by gradual loss of neurons and functions of the central nervous systems. Their course is usually severe, leading to high morbidity and subsequent inability of patients to independent functioning. Vast majority of neurodegenerative diseases is currently untreatable, and only some symptomatic drugs are available which efficacy is usually very limited. To develop novel therapies for this group of diseases, it is crucial to understand their pathogenesis and to recognize factors which can influence the disease course. One of cellular structures which dysfunction appears to be relatively poorly understood in the light of neurodegenerative diseases is tubulin cytoskeleton.

Microsoft’s update for Direct3D, with opacity micromaps and shader execution reordering now official features, will probably mean little to gamers but graphics devs are going to be happy

Which should make devs a little bit happier.

The Blood of Centenarians Reveals 37 Proteins Linked With Slower Aging

Science is one step closer to cracking the code of longevity thanks to a new study that identified dozens of proteins linked with slower aging in the blood of centenarians.

Scientists in Switzerland collected and compared blood samples from healthy younger individuals aged 30 to 60, hospitalized octogenarians aged 80 to 90, and centenarians aged 100 years and older, assessing how the expression of plasma proteins evolves and affects metabolism, immunity, and overall lifespan.

Of the more than 700 proteins measured, 37 formed a profile that was “closer to those of the youngest group than to those of octogenarians,” says Flavien Delhaes, cell physiologist at the University of Geneva and the study’s first author.

Mitochondrial Ca2+ efflux controls neuronal metabolism and long-term memory across species

Mitochondrial calcium regulates neuronal metabolism and memory.

Brain metabolism is important for long-term memories (LTMs) and various brain functions, Although it is well known that impairing neuronal metabolism limits brain performance, it is not clear if expanding the metabolic capacity of neurons boosts brain function.

In this study, the authors demonstrate that increasing mitochondrial metabolism can enhance LTM formation in flies and mice.

The authors increase mitochondrial Ca2+ by knocking down the mitochondrial Ca2+ exporter Letm1 and demonstrate over-activation of mitochondrial metabolism in neurons of central memory circuits, leading to improved LTM storage. sciencenewshighlights Science Mission https://sciencemission.com/Mitochondrial-Ca2-efflux

Boosting mitochondrial metabolism in neurons in central memory circuits by enhancing Ca2+ retention in the mitochondrial matrix is shown to improve long-term memory formation in flies and mice.

Accelerating and Streamlining Microbial Process Development

CDMO Fujifilm Biotechnologies unveiled its ShunzymeX precision purification technology, which is aimed at simplifying downstream processing for complex biologics. The technology will be presented this week at the Festival of Biologics conference in San Diego.

Fujifilm Biotechnologies, in collaboration with the University of Edinburgh, developed ShunzymeX, a proprietary technology that leverages a novel protease to enable purification of complex biologics with a simplified process, according to the company. This technology enables the addition of an affinity tag to the protein, allowing the biologic protein to be purified with an off-the-shelf affinity resin. After purification, the novel protease cleaves off the tag without leaving a scar on the native protein.

ShunzymeX addresses some of the inherent challenges in traditional microbial downstream purification due to the diversity of microbial-expressed proteins, including variability in size and sequence, leading to a lack of suitable affinity resins, says John Stewart, senior vice president of global process development, Fujifilm Biotechnologies.

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