Ceria nanoparticles (CeO₂NPs) exhibit great potential in cardiovascular disease and nonalcoholic fatty liver disease due to its excellent antioxidant capacity. However, the profitable effect of CeO₂NPs on many diseases is almost all attributed to the regulation of ROS. Apart from the general antioxidant function, there seems to be no more distinct mechanism to reflect its unique multi-disease improvement effect. Here, we for the first time reveal a new discovery of CeO₂NPs in mimicking nitric oxide synthase (NOS) by catalyzing L-arginine (L-Arg) to produce nitric oxide (NO) or the derivatives. NOS-like activity of CeO₂NPs is original and associated with multiple factors like substrate concentration, pH, temperature and time, etc. where oxygen vacancy ratio plays a more critical role. Meanwhile, NOS-like activity of CeO₂NPs successfully elevates NO secretion in endothelial cells and macrophages without expanding eNOS/iNOS expression. Importantly, NOS-like activity of CeO₂NPs and the responsive endogenous NO promote the re-distribution of blood lipids and stabilize eNOS expression but suppress iNOS, thus collectively alleviate the accumulation of vascular plaque. Altogether, we provide a new angle of view to survey the outstanding potential of CeO₂NPs, apart from the inevitable antioxidant capacity, the covert but possible and more critical NOS-like enzymatic activity is more noteworthy.

Metabolic dysfunction-associated steatotic liver disease (MASLD) can progress to metabolic dysfunction-associated steatohepatitis (MASH) and liver fibrosis, contributing to a heavier global health burden. Non-invasive diagnostic tools developed using machine learning (ML) and deep learning (DL), two representative artificial intelligence algorithms, are increasingly being explored for MASH and its related fibrosis assessment. This study aimed to compare the diagnostic performance of different ML and DL models and identify the top-performing models for diagnosing MASH and associated liver fibrosis. A systematic review and meta-analysis were conducted across PubMed, Web of Science, Embase and Cochrane Library from inception to May 18, 2025. Pooled area under the receiver operator characteristic curve (AUROC) values with 95 % confidence interval (CI) were calculated. Accuracy, specificity, sensitivity, positive predictive values, and negative predictive values were also recorded. Of 4,314 studies initially identified, 106 met the inclusion criteria, with 35 studies (ML: n = 28; DL: n = 7) providing data for analysis. Logistic Regression and Neural Network are the most commonly algorithms applied in ML and DL, respectively. The pooled AUROCs for diagnosing MASH were 0.833 (95 %CI: 0.806-0.860) for ML models and 0.841 (95 %CI: 0.782-0.900) for DL models. Light Gradient Boosting Machine (LightGBM) and ResNet50 were the best-performing models for diagnosing MASH within ML and DL algorithms, respectively, achieving corresponding AUROCs of 0.920 (95 %CI: 0.916-0.924) and 0.960 (95 %CI: 0.951-0.969). For fibrosis diagnosis, ML models had a pooled AUROC of 0.826 (95 %CI: 0.792-0.860), with Categorical Boosting (CatBoost) achieving the highest AUROC of 0.960 (95 %CI: 0.950-0.970). DL models yielded the pooled AUROC of 0.875 (95 %CI: 0.816-0.934) for fibrosis diagnosis. Both ML and DL models demonstrated strong diagnostic performance for MASH and liver fibrosis, with DL achieving marginally higher AUROCs. AI-driven approaches show promise in MASLD management.

Chronic myeloid leukemia (CML) is a malignant clonal disease of hematopoietic stem cells driven by the BCR-ABL fusion gene. Although tyrosine kinase inhibitors (TKIs) serve as targeted therapies, drug resistance remains one of the key challenges affecting the long-term survival of CML patients. A novel iron-based nano-reagent of Mn-Zn Ferrite was constructed to explore its role in regulating the redox homeostasis of CML cells and to clarify its therapeutic potential in reversing drug resistance in CML. CCK8 experiments were used to evaluate the effect of Mn-Zn Ferrite nanoparticles (Nano-Iron) on the drug sensitivity of adriamycin in K562 cells and adriamycin-resistant K562 cells (K562/ADR). Apoptosis, reactive oxygen species (ROS) levels, superoxide dismutase (SOD) levels in K562 cells and K562/ADR cells were measured after treatment of Nano-Iron and adriamycin. Further detection was conducted on the levels of glutathione (GSH), oxidized glutathione (GSSG) and GSH/GSSG ratio in K562 cells and K562/ADR cells after combined intervention. Meanwhile, the expression of glutathione peroxidase 4 (GPX4) and malondialdehyde (MDA) levels after combined intervention were determined. In vivo experiments involved in constructing systemic metastasis tumor models of K562 and K562/ADR in mice, which were treated with Nano-Iron and adriamycin. On the 10th, 15th and 20th day after tumor formation, in vivo imaging and medial canthal vein blood collection were performed to evaluate the proportion of tumor cells in peripheral blood. All mice were weighed regularly and euthanized when showing mental depression, at the same time, another batch of mice were used to calculate their survival period. Spleens and femurs were collected for hematoxylin–eosin (HE) and GPX4 staining. Mn Zn ferrite (Nano-Iron) enhances the sensitivity of K562/ADR cells to adriamycin. After co-treatment with Nano-Iron and adriamycin, more apoptosis of K562/ADR cells was induced and accompanied with an increase of ROS and MDA levels, as well as a decrease of GSH/GSSG ratio and GPX4 expression. In vivo experiments have shown that the combination therapy of Nano-Iron and adriamycin prolongs the survival period of mice, significantly inhibits the infiltration of tumor cells in the bone marrow and suppresses the expression of GPX4 in the femur of mice. Mn-Zn Ferrite (Nano-Iron) enhances the therapeutic sensitivity of K562/ADR cells to adriamycin by inducing ferroptosis, demonstrating the therapeutic potential in reversing drug resistance.

Background: Inflammatory bowel disease (IBD), characterized by chronic inflammation of the digestive tract, involves angiogenesis as a key pathogenic mechanism. Ginsenoside Rg3, derived from the traditional Chinese herb ginseng, is recognized for its anti-angiogenic properties but is limited by low oral bioavailability. This necessitates the development of an alternative delivery system to improve its therapeutic effectiveness. Methods: Pluronic F-127 (F127) and Pluronic F-68 (F68) were used to construct Rg3-loaded thermosensitive hydrogel Gel-Rg3. Meanwhile, a series of physicochemical properties were determined. Then the safety and pharmacological activity of Gel-Rg3 were evaluated in vitro and in vivo using human umbilical vein endothelial cells (HUVECs) and colitis mouse model, in order to initially validate the potential of Gel-Rg3 for the treatment of IBD. Results: We engineered a rectally administrable, thermosensitive Gel-Rg3 hydrogel using F127 and F68, which forms at body temperature, enhancing Rg3’s intestinal retention and slowly releasing the drug. In vitro, Gel-Rg3 demonstrated superior anti-angiogenic activity by inhibiting HUVEC proliferation, migration, and tube formation. It also proved safer and better suited for IBD’s delicate intestinal environment than unformulated Rg3. In vivo assessments confirmed increased intestinal adhesion and anti-angiogenic efficacy. Conclusions: The Gel-Rg3 hydrogel shows promise for IBD therapy by effectively inhibiting angiogenesis via rectal delivery, overcoming Rg3’s bioavailability limitations with improved safety and efficacy. This study provides new inspiration and data support for the design of treatment strategies for IBD.

The N-terminal 20 peptide of cementum matrix protein 1 (CEMP1) modified with glycine–proline–hydroxyproline shows an affinity for collagen.