Xiaohuan Yuan

Current injectable fillers often suffer from a transient efficacy and insufficient early stage improvement. To address this, we developed a composite dermal filler consisting of hyaluronic acid (HA) and poly-L-lactic acid-methoxypolyethyleneglycol (PLLA-mPEG) microspheres with a unique fibrous porous structure. This distinctive architecture enabled a rapid initial release of lactic acid, effectively accelerating early cell proliferation and fundamentally overcoming the challenge of poor initial skin improvement. In a rat model, the composite filler demonstrated superior performance by orchestrating a pro-regenerative microenvironment, eliciting controlled macrophage infiltration, upregulating TGF-β expression, and significantly stimulating endogenous collagen regeneration, which leads to sustained volume restoration. By ingeniously coupling the instant filling effect of HA with the structurally enhanced bioactive function of PLLA-mPEG microspheres, this composite filler represents a breakthrough strategy that synchronizes immediate correction with long-term tissue remodeling, holding great promise for treating skin laxity and soft tissue defects.

Wound healing in diabetes is a complicated and challenging task, which is affected by many factors. For example, microcirculatory disorders, inflammatory reactions, cell signaling disruption, abnormal fibrosis, and impaired immunity due to high blood sugar may have an adverse effect on wound healing. In order to address this problem, researchers have continued to explore a broad range of innovative approaches. Nanoparticles, as a novel repair material, are widely used due to their unique physical and chemical properties, particularly in the treatment of diabetes; however, they also have certain limitations. Cell membrane-coated nanoparticles, with their inherent biocompatibility and precise drug delivery capabilities, have emerged as a novel and highly effective strategy for treating diabetic wounds. Among these, nanoparticles coated with macrophage membranes and mesenchymal stem cell membranes have demonstrated the most significant therapeutic effects in wound anti-inflammation, vascular regeneration, and tissue repair. They can effectively improve the local pathological microenvironment, offering a novel and highly effective nanotherapeutic strategy for the treatment of chronic wounds. This paper systematically reviews research progress on nanoparticles coated with red blood cell membranes, macrophage membranes, stem cell membranes, and exosome membranes for treating diabetic wounds. It comprehensively organizes findings based on membrane source classification, mechanisms of action and in vitro/in vivo evidence. Compared to existing reviews, this paper’s primary innovations and contributions lie in establishing a comprehensive membrane classification system, deeply analyzing the synergistic logic of multi-mechanism actions, and it provides a comprehensive analysis of practical challenges in areas such as reproducibility, safety, immunomodulation, large-scale production, regulatory compliance, and clinical translation. It provides theoretical support and practical references for developing more precise and safer wound repair strategies in the future.

This study aims to validate the capability of inertial measurement units (IMUs) combined with surface electromyography (sEMG) sensors for assessing lumbar self-load. Lumbar biomechanical simulation was performed using OpenSim software, and data collected by IMUs and sEMG sensors were integrated into the simulation to evaluate the system’s performance in assessing lumbar load under static postures in real environments. In the experiment, 15 IMUs were fixed at human anatomical landmarks, and motion data and sEMG signals were synchronously collected during isometric tests of lumbar muscles. IMU data were converted into an OpenSim-compatible format through a self-developed processing workflow to realize musculoskeletal dynamic and kinematic analysis. The experiment included four types of static posture tests, and six sets of isometric test motion data were collected. The results showed that under different static postures, the L1–L5 lumbar joints remained stable, the distribution of joint driving torque showed a regular pattern, and the muscle driving forces were different and basically consistent with physiological reality; sEMG signal analysis verified the evaluation capability of the system, and the muscle fatigue characteristics were consistent with expectations. This study confirms the methodological effectiveness of the combination of IMU and sEMG sensors for static lumbar load assessment in real environments, providing a potential methodological reference for the clinical evaluation of nonspecific low back pain. Received: 21 November 2025 | Revised: 7 January 2026 | Accepted: 26 January 2026 Conflict of Interest The authors declare that they have no conflicts of interest to this work. Data Availability Statement Data are available from the corresponding author upon reasonable request. Author Contribution Statement Zhong Wang: Methodology, Software, Validation, Formal analysis, Investigation, Data curation, Writing – original draft, Visualization. Xiaohuan Yuan: Writing – review & editing, Supervision. Yuanliang Tang: Conceptualization, Resources, Writing – review & editing, Supervision. Shaohui Zhang: Conceptualization, Resources, Writing – review & editing, Supervision, Project administration, Funding acquisition.

To advance the perception capabilities of flexible robotic arms, this study integrates sensing capabilities into a hybrid design combining conductive fabric with a “twisted tower” origami structure. This approach enables the creation of flexible structural units that combine flexibility, reconfigurability, and sensing-deformation feedback capabilities. Through experiments and simulations, we analyzed the effects of manufacturing processes, mechanical properties, electrical responses, and layer count on sensing performance. Our results demonstrated a positive correlation between displacement and load under static conditions, accompanied by stable and synchronized sensing signals. We also found that the layer count significantly modulated structural stiffness, load-bearing capacity, and sensing sensitivity. Furthermore, stable resistance changes observed during deformation validated the sensing reliability, and stress-strain simulations effectively revealed the correlation between deformation and sensing signals.

Purpose: Nanovesicles (NVs) derived from bone mesenchymal stem cells (BMSCs) as drug delivery systems are considered an effective therapeutic strategy for diabetes. However, its mechanism of action remains unclear. Here, we evaluated the efficacy and molecular mechanism of BMSC-derived NVs carrying the curcumin analog H8 (H8-BMSCs-NVs) on hepatic glucose and lipid metabolism in type 2 diabetes (T2D). Subjects and Methods: Mouse BMSCs were isolated by collagenase digestion and H8-BMSCs-NVs were prepared by microvesicle extrusion. The effects of H8-BMSCs-NVs on hepatic glucose and lipid metabolism were observed in a T2D mouse model and a HepG2 cell insulin resistance model. To evaluate changes in potential signaling pathways, the PI3K/AKT/AMPK signaling pathway and expression levels of G6P and PEPCK were assessed by Western blotting. Results: H8-BMSCs-NVs effectively improved lipid accumulation in liver tissues and restored liver dysfunction in T2D mice. Meanwhile, H8-BMSCs-NVs effectively inhibited intracellular lipid accumulation in the insulin resistance models of HepG2 cells. Mechanistic studies showed that H8-BMSCs-NVs activated the PI3K/AKT/AMPK signaling pathway and decreased the expression levels of G6P and PEPCK. Conclusion: These findings demonstrate that H8-BMSCs-NVs improved hepatic glucose and lipid metabolism in T2D mice by activating the PI3K/AKT/AMPK signaling pathway, which provides novel evidence suggesting the potential of H8-BMSCs-NVs in the clinically treatment of T2D patients.

Diabetic wound healing remains a worldwide challenge for both clinicians and researchers. The high expression of matrix metalloproteinase 9 (MMP9) and a high inflammatory response are indicative of poor diabetic wound healing. H8, a curcumin analogue, is able to treat diabetes and is anti-inflammatory, and our pretest showed that it has the potential to treat diabetic wound healing. However, H8 is highly expressed in organs such as the liver and kidney, resulting in its unfocused use in diabetic wound targeting. (These data were not published, see Table S1 in the Supporting Information.) Accordingly, it is important to pursue effective carrier vehicles to facilitate the therapeutic uses of H8. The use of H8 delivered by macrophage membrane-derived nanovesicles provides a potential strategy for repairing diabetic wounds with improved drug efficacy and fast healing. In this study, we fabricated an injectable gelatin microsphere (GM) with sustained MMP9-responsive H8 macrophage membrane-derived nanovesicles (H8NVs) with a targeted release to promote angiogenesis that also reduces oxidative stress damage and inflammation, promoting diabetic wound healing. Gelatin microspheres loaded with H8NV (GMH8NV) stimulated by MMP9 can significantly facilitate the migration of NIH-3T3 cells and facilitate the development of tubular structures by HUVEC in vitro. In addition, our results demonstrated that GMH8NV stimulated by MMP9 protected cells from oxidative damage and polarized macrophages to the M2 phenotype, leading to an inflammation inhibition. By stimulating angiogenesis and collagen deposition, inhibiting inflammation, and reducing MMP9 expression, GMH8NV accelerated wound healing. This study showed that GMH8NVs were targeted to release H8NV after MMP9 stimulation, suggesting promising potential in achieving satisfactory healing in diabetic treatment.

Diabetic wounds pose a significant challenge to public health, primarily due to insufficient blood vessel supply, bacterial infection, excessive oxidative stress, and impaired antioxidant defenses. The aforementioned condition not only places a significant physical burden on patients’ prognosis, but also amplifies the economic strain on the medical system in treating diabetic wounds. Currently, the effectiveness of available treatments for diabetic wounds is limited. However, there is hope in the potential of metal nanoparticles (MNPs) to address these issues. MNPs exhibit excellent anti-inflammatory, antioxidant, antibacterial and pro-angiogenic properties, making them a promising solution for diabetic wounds. In addition, MNPs stimulate the expression of proteins that promote wound healing and serve as drug delivery systems for small-molecule drugs. By combining MNPs with other biomaterials such as hydrogels and chitosan, novel dressings can be developed and revolutionize the treatment of diabetic wounds. The present article provides a comprehensive overview of the research progress on the utilization of MNPs for treating diabetic wounds. Building upon this foundation, we summarize the underlying mechanisms involved in diabetic wound healing and discuss the potential application of MNPs as biomaterials for drug delivery. Furthermore, we provide an extensive analysis and discussion on the clinical implementation of dressings, while also highlighting future prospects for utilizing MNPs in diabetic wound management. In conclusion, MNPs represent a promising strategy for the treatment of diabetic wound healing. Future directions include combining other biological nanomaterials to synthesize new biological dressings or utilizing the other physicochemical properties of MNPs to promote wound healing. Synthetic biomaterials that contain MNPs not only play a role in all stages of diabetic wound healing, but also provide a stable physiological environment for the wound-healing process.

Accumulating evidence indicates that cellular premature senescence of the glomerulus, including endothelial cells, mesangial cells, and podocytes leads to diabetic nephropathy (DN), and DN is regarded as a clinical model of premature senescence. However, the role of cellular senescence‐associated genes in the glomerulus in DN progression remains unclear. Therefore, this work aims to identify and validate potential cellular aging‐related genes in the glomerulus in DN to provide novel clues for DN treatment based on anti‐aging. The microarray GSE96804 dataset, including 41 diabetic glomeruli and 20 control glomeruli, is retrieved from the Gene Expression Omnibus (GEO) database and cellular senescence‐related genes (CSRGs) are obtained from the GeneCards database and literature reports. Subsequently, PPI, GO, and KEGG enrichment are analyzed by screening the intersection between differentially expressed genes (DEGs) and CSRGs. scRNA‐seq dataset GSE127235 is used to verify core genes expression in glomerulocytes of mice. Finally, db/db mice are utilized to validate the hub gene expression in the glomeruli, and high glucose‐induced mesangial cells are used to confirm key gene expression. This study reveals that FOS and ZFP36 may play an anti‐aging role in DN to ameliorate cell intracellular premature aging in mesangial cells of glomeruli.

Excessive production of transforming growth factor β1 (TGF-β1) in activated hepatic stellate cells (aHSCs) promotes liver fibrosis by activating the TGF-β1/Smad signaling pathway. Thus, specifically inhibiting the pro-fibrotic activity of TGF-β1 in aHSCs is an ideal strategy for treating liver fibrosis. Overexpression of platelet-derived growth factor β receptor (PDGFβR) has been demonstrated on the surface of aHSCs relative to normal cells in liver fibrosis. Interferon-gamma peptidomimetic (mIFNγ) and truncated TGF-β receptor type II (tTβRII) inhibit the TGF-β1/Smad signaling pathway by different mechanisms. In this study, we designed a chimeric protein by the conjugation of (1) mIFNγ and tTβRII coupled via plasma protease-cleavable linker sequences (FNPKTP) to (2) PDGFβR-recognizing peptide (BiPPB), namely BiPPB-mIFNγ-tTβRII. This novel protein BiPPB-mIFNγ-tTβRII was effectively prepared using Escherichia coli expression system. The active components BiPPB-mIFNγ and tTβRII were slowly released from BiPPB-mIFNγ-tTβRII by hydrolysis using the plasma protease thrombin in vitro. Moreover, BiPPB-mIFNγ-tTβRII highly targeted to fibrotic liver tissues, markedly ameliorated liver morphology and fibrotic responses in chronic liver fibrosis mice by both inhibiting the phosphorylation of Smad2/3 and inducing the expression of Smad7. Meanwhile, BiPPB-mIFNγ-tTβRII markedly reduced the deposition of collagen fibrils and expression of fibrosis-related proteins in acute liver fibrosis mice. Furthermore, BiPPB-mIFNγ-tTβRII showed a good safety performance in both liver fibrosis mice. Taken together, BiPPB-mIFNγ-tTβRII improved the in vivo anti-liver fibrotic activity due to its high fibrotic liver-targeting potential and the dual inhibition of the TGF-β1/Smad signaling pathway, which may be a potential candidate for targeting therapy on liver fibrosis.

Cardiac fibrosis is a remodeling process of the cardiac interstitium, characterized by abnormal metabolism of the extracellular matrix, excessive accumulat