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Senovax takes a novel approach

Senescent “zombie” cells accumulate as we age, releasing inflammatory signals that damage surrounding tissue. Senovax takes a novel approach: train the immune system to recognize these cells and eliminate them. By exposing dendritic immune cells to lab-generated senescent cells, the body learns the markers that identify aging cells. The result: the immune system creates a “wanted poster” and begins targeting senescent cells throughout the body. Unlike drugs that must reach specific tissues, the immune system already travels everywhere — and it remembers. One treatment could potentially provide long-lasting protection.

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A new way to deliver antibodies could make treatment much easier for patients

Antibody treatments for cancer and other diseases are typically delivered intravenously, because of the large volumes that are needed per dose. This means the patient has to go to a hospital for every treatment, where they may spend hours receiving the infusion.

MIT engineers have now taken a major step toward reformulating antibodies so that they can be injected using a standard syringe. The researchers found a way to create solid particles of highly concentrated antibodies, suspended in a solution. These particles carry enough antibodies that only about 2 milliliters of solution would be needed per dose.

This advance could make it much easier for patients to receive antibody treatments, and could make treatment more accessible for patients who have difficulty coming into a hospital, including older people.

The Immune Cell Atlas of “Longevity Molecular Tag”: Identification of Principal Immune Cell Subsets and Their Underlying Molecular Regulatory Mechanisms

Immunosenescence represents a critical aspect of the aging process. Centenarians, serving as a nature model of “healthy aging,” demonstrate a distinctive immune “compensatory adaptation” mechanism that contributes to the maintenance of immune homeostasis. However, the specific immune cell subsets involved and the molecular mechanisms underlying these phenotypic traits remain incompletely understood. In this study, we integrated single-cell RNA sequencing data spanning the entire lifespan of East Asian populations with bulk transcriptomic data from a centenarian cohort in Guangxi. Utilizing the Scissor algorithm, we identified immune cell subpopulations positively (Scissor+) and negatively (Scissor−) associated with longevity phenotypes, thereby constructing an immune cell atlas of “Longevity Molecular Tag.” Our findings indicate that Scissor+ cells predominantly comprise natural killer (NK) cells, CD8+ T cells, and γδ T cells, characterized by enhanced cytotoxic and immunomodulatory functions. Conversely, Scissor− cells mainly include CD4+ T cells, B cells, and dendritic cells (DCs), which are linked to inflammatory signaling pathways and Th17/Th1 differentiation. Trajectory analysis elucidated the differentiation pathways of NK, CD8+ T cells, CD4+ T cells, and B cells. Differentially expressed genes were enriched in pathways such as NF-κB signaling, T cell receptor signaling, and NK cell cytotoxicity. Furthermore, co-localization analysis revealed five eQTL-colocalized events (rs3793537–GLIPR2/CD72/TLN1 and rs8019902–TRDV2/TRDC) associated with longevity. Collectively, these results suggest that centenarians achieve immune equilibrium by remodeling cytotoxic immune lineages and finely tuning inflammatory responses, thereby promoting health span and longevity. This study offers novel insights into potential strategies for modulating immunosenescence.

The Strehler-Mildvan mortality correlation arises from changes in the variability of ageing

As global human life expectancy continues to rise, accompanying increases in healthspan that prevent morbidity expansion become increasingly imperative. Population lifespan can increase in distinct ways, for instance through rectangularisation (steepening) or triangularisation (flattening) of survival curves. These two demographic changes, particularly rectangularisation, occur frequently across human and model organism populations, yet their biological determinants and effects on healthspan and morbidity are largely unknown. Notably, these modes of life-extension occur when parameters of the Gompertz mortality model (capturing exponential age-increases in mortality rate) change inversely, a widely-reported phenomenon known as the Strehler-Mildvan correlation — whose biological basis also remains unexplained. We therefore investigated longitudinal health, morbidity and lifespan in 30 Caenorhabditis elegans cohorts using multiple life-extension protocols. We report that survival curve rectangularisation results from healthspan expansion in short-lived population members, whereas triangularisation from healthspan and morbidity expansion in long-lived population members. Interestingly, rectangularisation and triangularisation respectively decrease and increase inter-individual variation in the ageing process, and the mode of life-extension that occurs depends on levels of existing variation. Notably, triangularisation was more effective at extending lifespan without morbidity expansion. Analysis of fruit fly and mouse data show that these biological determinants of the Strehler-Mildvan correlation are also largely evolutionarily conserved.

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Decreased Glucose Metabolism and Declined Chaperones Are Unique Features Required for the Survival of Senescent Fibroblasts and Pyruvate Dehydrogenase Is a Potent Senolytic Target

By a global proteomic profiling of senescent human BJ fibroblasts induced by ionizing radiation, 178 cellular proteins with at least 4-fold or greater changes in abundance were identified, representing the cellular landscape of the senescent fibroblasts. Functional enrichments and biological experiments demonstrated that the decreased glucose metabolism, reduced ATP and alpha-KG production, and declined chaperones are the most striking features associated with senescent fibroblasts. Moreover, these proteomic features are closely correlated with their transcription alterations confirmed by RT-PCR. Respectively, inhibiting pyruvate dehydrogenase (critical enzyme to supply acetyl-CoA to TCA cycle) or glutaminase GLS1 (crucial enzyme to supplement TCA cycle intermediate alpha-KG) or inhibiting Hsp90 (important member of chaperones) led to the selective killing of senescent fibroblasts, indicating the essential roles of the TCA cycle or chaperones in the survival and maintenance of cellular senescence. Most importantly, co-inhibiting the TCA cycle and Hsp90 gave rise to the enhanced selective killing of senescent fibroblasts as well as the therapy-induced senescent cancer cells and the alleviation of physical dysfunctions in aged mice, suggesting the synergistic regulation of cellular senescence by the TCA cycle and chaperones. Thus, our profiling revealed key cellular features for the survival and maintenance in senescent normal cells, demonstrating that pyruvate dehydrogenase is a novel and potent senolytic target for the selective elimination of senescence.

Scientists Find Protein Inside The Body That Reverses Brain Aging

Cyclin D-binding myb-like transcription factor 1 or DMTF1a key protein in the brain can help to regenerate neural stem cells and improve aging-associated memory decline. NUS scientists found that this protein’s levels are repressed in the “aged” neural stem cells, Health & Wellness News, Health and Me

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.

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