Zhizhun Mo

The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway can recognize pathogen-derived and host DNA. This factor triggers innate immune responses and thereby establishes a broad and effective surveillance mechanism for tissue damage and pathogen invasion. In acute pancreatitis (AP), the cGAS-STING signaling pathway exerts diverse regulatory functions during the process of pancreatic cell death. We systematically review the molecular mechanism of the cGAS-STING signaling pathway in acute pancreatitis. We summarize the latest research progress on the interaction of this pathway with various forms of programmed cell death. Through specific case analyses, we elaborate on the key role of the cGAS-STING signaling pathway in regulating apoptosis, autophagy, ferroptosis, pyroptosis and inflammatory responses. Finally, this article also explores the potential research value of several natural plant-derived compounds. They achieve this by regulating this pathway and thereby interfering with the mechanism of cell death during the pathological process of acute pancreatitis.

Ischemic stroke is a leading cause of death and disability, with limited therapies beyond reperfusion. CD147 (Basigin), upregulated after cerebral ischemia, participates in neuroinflammation, however, its precise contributions to blood-brain barrier (BBB) disruption and neuronal injury are incompletely understood. Using a photothrombotic permanent middle cerebral artery occlusion (pMCAO) model in C57BL/6J male adult mice, we delivered CD147-overexpressing adenovirus (Ad Bsg) or control fluorophore adenovirus (Ad Fc) via intracerebroventricular injection. Infarct volume, neurological deficits, motor function, neuronal apoptosis, BBB integrity and hemorrhagic transformation were assessed. In vitro, HT22 neuronal cells were treated with recombinant Cyclophilin A (CyPA) to activate CD147 signaling. Wnt/β-catenin pathway activity was evaluated by western blot and qPCR. Using constitutively active β-catenin mice and pharmacological activation of AKT (using SC-79) were also performed. CD147 expression peaked at 24 h after stroke and correlated with infarct volume and neurological deficit severity. CD147 overexpression significantly increased infarct size, neuronal apoptosis, BBB leakage, brain edema, and downregulated the expression of claudin-5 and ZO-1. In neurons, CyPA-induced CD147 activation reduced p-AKT, p-GSK3β, β-catenin, and Wnt target gene expression. These effects were reversed by CD147 knockdown or by constitutively active β-catenin. CD147 exacerbates ischemic brain injury and BBB disruption by suppressing neuronal Wnt/β-catenin signaling through a mechanism involving the AKT/GSK3β node, supporting further evaluation of CD147-directed interventions after stroke.

Background: Influenza viruses cause approximately 3 to 5 million severe cases and tens of thousands of deaths globally each year, posing a continuous threat to public health. Nanoparticles with superior biocompatibility, combined with traditional Chinese herbal medicine could offer promising avenues to enhance therapeutic efficacy, improve targeting precision, and address multidrug resistance. This study aims to provide a comprehensive review of the current status and future directions of nanoparticle applications in influenza research, thereby providing more effective and convenient solutions for influenza prevention and control. Methods: A publication search was performed using Web of Science Core Collection, Scopus, and PubMed from 2005 to 2025 to improve the completeness of publications collection. Bibliometric analyses performed using Bibliometrix, CiteSpace, and VOSviewer software to compensate for the differences in their respective algorithms. The analysis by evaluating publication quantity, Citation Counts, and Co-authorship status to find the core institutions, journals, and key authors. Explore the research hotspots of nanoparticles and influenza through keyword analysis. Result: A total of 3,478 relevant publications were identified. The United States and China were the primary contributors in terms of publication volume, with the Chinese Academy of Sciences leading in institutional contributions. Vaccines emerged as the top-performing journal in this field. Masaru Kanekiyo’s article had the highest local citation count, and he was identified as the author with the greatest individual contribution. Keyword analysis revealed that optimizing delivery systems and advancing vaccine development are central research priorities. Notably, bibliometric analysis revealed that besides metal-based nanoparticles, viral-like particles, polymer nanoparticles, and lipid nanoparticles in the field of delivery system research, herbal small-molecule nanoparticle delivery system has garnered significant attention due to the promise for future clinical applications. Conclusion: Research on nanoparticles in influenza is rapidly advancing, with a primary focus on their application in vaccine development and delivery optimization. The field is also exploring nanoparticles from various sources. Future research should bridge basic mechanistic studies with clinical applications to enhance their impact.

Snakebite envenomation requires rapid venom identification for effective treatment, a need unmet by current diagnostics in China. This study aimed to develop a rapid, multiplex immunofluorescence lateral flow assay for the simultaneous detection of four major venomous snakes: Deinagkistrodon acutus, Bungarus multicinctus, Naja atra , and Agkistrodon halys . Key findings demonstrated that the assays exhibited high sensitivity, with limits of detection (LODs) ranging from 0.6 to 1.2 ng/mL. Excellent specificity was confirmed, with no cross‐reactivity observed among the four venoms. In a rabbit envenomation model, the assays accurately quantified venom in various biological samples (venous serum, wound exudate) within 5 min. Receiver operating characteristic (ROC) curve analysis showed high diagnostic accuracy, with areas under the ROC curve (AUCs) ranging from 0.889 to 0.956. Assay accuracy was further verified by spike‐in recovery rates of 90.3%–109.6%. The results indicate that this novel multiplex immunoassay shows great potential as a point‐of‐care tool for the rapid and quantitative diagnosis of snakebites, showing great potential for preclinical application following further human sample validation.

The initial stages of acute pancreatitis (AP) are characterized by a significant event - acinar ductal metaplasia (ADM). This process is a crucial feature of both acute and chronic pancreatitis, serving as the first step in the development of pancreatic cancer. Ion channels are integral transmembrane proteins that play a pivotal role in numerous biological processes by modulating ion flux. In many diseases, the expression and activity of ion channels are often dysregulated. Metal ions, including calcium ions (Ca²⁺), ferrous ions (Fe²⁺), and Copper ions (Cu²⁺), assume a distinctive role in cellular metabolism. These ions possess specific biological properties relevant to cellular function. However, the interactions among these ions exacerbate the imbalance within the intracellular environment, resulting in cellular damage and influencing the progression of AP. A more in-depth investigation into the mechanisms by which these ions interact with acinar cells is essential for elucidating AP’s pathogenesis and identifying novel therapeutic strategies. Currently, treatment for AP primarily focuses on pain relief, complications prevention, and prognosis improvement. There are limited specific treatments targeting acinous cell dedifferentiation or ion imbalance. This study aims to investigate potential therapeutic strategies by examining ion crosstalk within acinar cells in the context of acute pancreatitis.

Ischemic stroke, accounting for the majority of stroke events, significantly contributes to global morbidity and mortality. Vascular recanalization therapies, namely intravenous thrombolysis and mechanical thrombectomy, have emerged as critical interventions, yet their success hinges on timely application and patient‐specific factors. This review focuses on the early phase pathophysiological mechanisms of ischemic stroke and the nuances of recanalization. It highlights the dual role of neutrophils in tissue damage and repair, and the critical involvement of the blood–brain barrier (BBB) in stroke outcomes. Special emphasis is placed on ischemia–reperfusion injury, characterized by oxidative stress, inflammation, and endothelial dysfunction, which paradoxically exacerbates cerebral damage post‐revascularization. The review also explores the potential of targeting molecular pathways involved in BBB integrity and inflammation to enhance the efficacy of recanalization therapies. By synthesizing current research, this paper aims to provide insights into optimizing treatment protocols and developing adjuvant neuroprotective strategies, thereby advancing stroke therapy and improving patient outcomes.

Alzheimer’s disease (AD) is one of the most common progressive neurodegenerative diseases, accompanied by global alterations in metabolic profiles. In the past 10 years, over hundreds of metabolomics studies have been conducted to unravel metabolic changes in AD, which provides insight into the identification of potential biomarkers for diagnosis, treatment, and prognostic assessment. However, since different species may lead to systemic abnormalities in metabolomic profiles, it is urgently needed to perform a comparative metabolomics analysis between AD animal models and human patients. In this study, we integrated 78 metabolic profiles from public literatures, including 11 metabolomics studies in different AD mouse models and 67 metabolomics studies from AD patients. Metabolites and enrichment analysis were further conducted to reveal key metabolic pathways and metabolites in AD. We totally identified 14 key metabolites and 16 pathways that are both differentially significant in AD mouse models and patients. Moreover, we built a metabolite-target network to predict potential protein markers in AD. Finally, we validated HER2 and NDF2 as key protein markers in APP/PS1 mice. Overall, this study provides a comprehensive strategy for AD metabolomics research, contributing to understanding the pathological mechanism of AD.