Bioactive Materials
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2024
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IF 18
Jiayi Yuan,Bingbing Sun,Weixing Ma,Chao Cai,Zhenzhen Huang,Peiyi Zhou,Lei Yi,Lubin Liu,Shixuan Chen
Repairing large-area soft tissue defects caused by traumas is a major surgical challenge. Developing multifunctional scaffolds with suitable scalability and favorable cellular response is crucial for soft tissue regeneration. In this study, we developed an orthogonally woven three-dimensional (3D) nanofiber scaffold combining electrospinning, weaving, and modified gas-foaming technology. The developed orthogonally woven 3D nanofiber scaffold had a modular design and controlled fiber alignment. In vitro, the orthogonally woven 3D nanofiber scaffold exhibited adjustable mechanical properties, good cell compatibility, and easy drug loading. In vivo, for one thing, the implantation of an orthogonally woven 3D nanofiber scaffold in a full abdominal wall defect model demonstrated that extensive granulation tissue formation with enough mechanical strength could promote recovery of abdominal wall defects while reducing intestinal adhesion. Another result of diabetic wound repair experiments suggested that orthogonally woven 3D nanofiber scaffolds had a higher wound healing ratio, granulation tissue formation, collagen deposition, and re-epithelialization. Taken together, this novel orthogonally woven 3D nanofiber scaffold may provide a promising and effective approach for optimal soft tissue regeneration.
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Biomolecules
·
2024
·Vol. 14
·期 8
·907
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IF 4.8
Yusu Wang,Ying Zong,Weijia Chen,Naichao Diao,Quanmin Zhao,Chunyi Li,Boyin Jia,Miao Zhang,Jianming Li,Yan Zhao,Rui Du,Zhongmei He
Due to the limited supply of autologous bone grafts, there is a need to develop more bone matrix materials to repair bone defects. Xenograft bone is expected to be used for clinical treatment due to its exact structural similarity to natural bone and its high biocompatibility. In this study, decellularized antler cancellous bone matrix (DACB) was first prepared, and then the extent of decellularization of DACB was verified by histological staining, which demonstrated that it retained the extracellular matrix (ECM). The bioactivity of DACB was assessed using C3H10T1/2 cells, revealing that DACB enhanced cell proliferation and facilitated cell adhesion and osteogenic differentiation. When evaluated by implanting DACB into nude mice, there were no signs of necrosis or inflammation in the epidermal tissues. The bone repair effect of DACB was verified in vivo using sika deer during the antler growth period as an animal model, and the molecular mechanisms of bone repair were further evaluated by transcriptomic analysis of the regenerated tissues. Our findings suggest that the low immunogenicity of DACB enhances the production of bone extracellular matrix components, leading to effective osseointegration between bone and DACB. This study provides a new reference for solving bone defects.
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REACTIVE & FUNCTIONAL POLYMERS
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2025
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IF 5.1
Lei Chen,Yin Lu,Kan Zhang
With the increasing awareness of environmental protection, considerable efforts are now devoted into bio-derived material fabrication. Through utilization of renewable biomass aligning with green chemistry principles, various sustainable materials have been prepared. In the current study, an innovative benzoxazine monomer containing dual coumarin moieties was successfully prepared through Mannich condensation using 4-methylumbelliferone (bio-phenolic precursor) and 7-amino-4-methylcoumarin (bio-amine component). The molecular architecture integrates photoreactive coumarin moieties, enabling dual photo-thermal curing capability. Structural validation via 1 H/ 13 C NMR and FT-IR spectroscopy confirmed the monomer integrity. Real-time UV–Vis spectroscopy monitoring indicated an 81 % conversion of the [2π + 2π] cycloaddition reaction following 2 h of UV irradiation (λ = 365 nm). The photopolymerized benzoxazine precursor shows a 5.4 °C curing temperature depression comparing to unphotopolymerized monomer. Complementary in-situ FT-IR analyses and DSC elucidated thermal-initiated ring-opening polymerization, demonstrating temperature-dependent conversion profiles. The polybenzoxazine prepared through photo-thermal polymerization shows higher thermal stability than solely thermal polymerized one. Through molecular design, this work realizes photo-thermal synergistic curing of bio-based benzoxazine resins, proposing an innovative approach to develop thermosetting materials that integrate low-energy processing, high heat resistance, and environmental sustainability.
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Exploration
·
2026
·
IF 30.4
Meng Sun,Fang Fang,Juan Liu,Yueyun Fan,Sa Wang,Chuang Zhang,Weiyu Li,Zhengyang Quan,Dongxu Zhao,Min Hu,Jinfeng Zhang
Acute liver failure (ALF), characterized by severe hepatocyte necrosis with a high mortality rate, remains a major global health challenge. However, there are currently no effective drug options for the clinical treatment of ALF. Herein, inspired by the new concept of a full-API nanodrug (FAND), we have rationally developed a quadruplex bioactive FAND (termed FAND HP@FuEVs ) composed entirely of active pharmaceutical ingredients (APIs). This FAND HP@FuEVs is constructed from fusion extracellular vesicles (FuEVs), which hybridize M2 macrophage-derived EVs (M2–EVs) with mesenchymal stem cell-derived EVs (MSC-EVs) and is subsequently engineered with two clinically therapeutic biomacromolecules: hepatocyte growth factor (HGF) and polyene phosphatidylcholine (PPC). Notably, FAND HP@FuEVs efficiently targets the damaged liver, benefiting from the dual inherent inflammation-tropism of the FuEVs. Moreover, FAND HP@FuEVs harnesses quadruplex biological activities by leveraging four natural bioactive components—M2-EVs, MSC-EVs, HGF, and PPC—to deliver pleiotropic therapies, including antioxidant, anti-inflammatory, pro-regenerative, and macrophage repolarization effects. These therapies are effective in treating ALF induced by both acetaminophen and hepatectomy, demonstrating significant clinical relevance based on data from patients with liver disease. Overall, the utilization of naturally derived or clinically approved APIs to construct full-bioactive nanodrugs creates opportunities for clinical translation as a safe, versatile, and multifaceted treatment for ALF.
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JOURNAL OF DRUG DELIVERY SCIENCE AND TECHNOLOGY
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2026
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IF 5.2
Xiaoxi Gao,Dehai Hou,Tianyu Ma,Sizhuo Liu,Ruiping Wang,Yang Ping,Jin Su
A synergistic nano-strategy co-delivering sorafenib and berberine to overcome resistance and reduce toxicity. • Optimized nanostructured lipid carriers with high drug loading, sustained release, and good stability were successfully prepared. • Pharmacokinetics showed significantly enhanced oral bioavailability (4.59-fold and 2.28-fold for SORB and BBR). • Superior antitumor efficacy and biosafety were systematically verified both in vitro and in vivo. Sorafenib (SORB) is a first-line drug for advanced hepatocellular carcinoma, but its clinical use is limited by poor water solubility, low oral bioavailability, and drug resistance. Berberine (BBR) has been shown to reverse multidrug resistance and enhance drug sensitivity. Here, we designed a nanostructured lipid carrier co-loaded with SORB and BBR (SBER NLC). The optimized formulation had a particle size of 123.17 ± 3.28 nm, PDI of 0.211 ± 0.012, and zeta potential of −18.30 ± 0.95 mV. Encapsulation efficiencies were 78.77 ± 0.93% (SORB) and 79.58 ± 1.04% (BBR), with drug loadings of 1.75 ± 0.06% and 1.28 ± 0.13%, respectively. SBER NLC showed stable storage properties and sustained release in simulated gastrointestinal fluids. Pharmacokinetic studies demonstrated significantly enhanced oral bioavailability of both drugs compared with free drug suspension. In vitro, SBER NLC exhibited stronger cytotoxicity and migration inhibition against HepG2 cells, while the blank carrier was nontoxic. In a HepG2 xenograft mouse model, SBER NLC achieved the strongest tumor suppression without causing body weight loss or major organ damage, and induced extensive nuclear pyknosis and necrosis in tumor tissue. This study provides an efficient nano-delivery strategy for combined SORB and BBR in hepatocellular carcinoma treatment. Download: Download high-res image (226KB) Download: Download full-size image
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BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
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2026
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IF 4.3
Leilei Qin,Yanli Guo,Yi Zhang,Nianting Tong,Chunning Zhao
Ribosomal L1 domain-containing protein 1 (RSL1D1) is an RNA-binding protein that relates to senescence. Nevertheless, the mechanism of RSL1D1 in modulating senescence and ferroptosis in diabetic retinopathy (DR) remains undefined. The DR mice were developed by intraperitoneal injection of STZ, and AAV targeting RPE was used for gene intervention. ARPE-19 cells were infected using oe-RSL1D1 and sh-FTH1 lentivirus before 30 mM high glucose (HG) exposure. Cell damage was assessed by measuring the expression of senescence and ferroptosis markers in ARPE-19 cells, along with oxidative stress indicators and Fe 2+ levels. RSL1D1 and FTH1 expression were significantly reduced in the retinal pigment epithelium (RPE) layer of diabetic mice and HG-induced ARPE-19 cells. Downregulation of RSL1D1 led to RPE cell senescence and dysregulated iron homeostasis-induced ferroptosis. HG treatment reduced the interaction between RSL1D1 protein and FTH1 mRNA in ARPE-19 cells, while RSL1D1 overexpression enhanced this interaction, thereby stabilizing FTH1 mRNA expression. The alleviating effects of RSL1D1 overexpression on retinal pigment epithelium cell senescence and ferroptosis in vitro and in vivo were compromised by FTH1 knockdown. Overall, this study unveils a posttranscriptional regulation of FTH1 by RSL1D1 and uncovers the implication of RSL1D1/FTH1 in cellular senescence and ferroptosis in DR.
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Scientific Reports
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2026
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IF 4.9
Qian Jingyu,Tang Xiaoyun,Ye Longji,Jin Panpan,Qin Zhongqiang,Wang Rongxin,Guo Hongyan,Li Miao
The development of hepatocellular carcinoma may be regulated by exosome-mediated cell-cell communication. GPC1-enriched exosomes have been associated with malignant phenotypes, while AQP1 has been related to tumor development and metastasis. The functional association of AQP1 and exosomal GPC1 in vivo remains to be clarified. Co-immunoprecipitation was applied to test the interaction of AQP1 with exosomal GPC1 in HCC cells. We generated a mouse xenograft model using control cells and AQP1 knockdown cells, with or without treatment with GPC1-high exosomes. Tumor growth was monitored by longitudinal caliper measurements and endpoint tumor weight. Histology and molecular characteristics were profiled using H&E staining, immunofluorescence, and immunohistochemistry. The proteins associated with ERK and MEK signaling pathways were detected through western blotting. Co-immunoprecipitation of AQP1 and GPC1 demonstrated a recovery of AQP1 and exosomal GPC1 in the same protein complex. AQP1 knockdown was accompanied by reduced xenograft tumor growth, and diminished tumor-promoting effect of GPC1-high exosomes. Tissue examinations revealed coordinated alterations in marker expression and proliferative state in all treatment groups. Total ERK and total MEK were largely similar across groups; phospho-ERK and phospho-MEK display condition-specific differences. Tumor AQP1 staining was markedly greater than that of peritumoral tissue. These data suggest that the AQP1 status may influence tumor sensitivity to GPC1 enriched exosomal stimulation in vivo, and suggest that further analysis of AQP1 as an effector in exosome related oncogenic activity in HCC is warranted.
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MOLECULAR AND CELLULAR BIOCHEMISTRY
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2026
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IF 4.7
Jiang Ling,Zhang Xiaolin,Dai Meng,Bi Ying,Han Lingling,Tao Xiaofeng,Wang Qi
Metastasis is the leading cause of death in patients with lung adenocarcinoma (LUAD), highlighting the urgent need to identify novel therapeutic targets. GLIS family zinc finger 1 (GLIS1) is a transcription factor implicated in multiple cancers. However, its role in LUAD remains poorly defined. In this study, we first identified that GLIS1 was significantly upregulated in LUAD tissues. To modulate its expression, lentiviral vectors were constructed to knock down or overexpress GLIS1 in NCI-H1975 and A549 LUAD cell lines, respectively. In vitro gain- and loss-of-function experiments revealed that GLIS1 knockdown significantly inhibited the migratory and invasive capabilities of NCI-H1975 cells. Conversely, GLIS1 overexpression enhanced these malignant phenotypes in A549 cells. In vivo study demonstrated that GLIS1 knockdown substantially reduced liver and lung metastasis of NCI-H1975 cells in mice. Furthermore, we found that downregulation of GLIS1 suppressed LUAD cell migration by inhibiting Homeobox A9 (HOXA9) methylation, which led to the subsequent upregulation of HOXA9 expression. Mechanistically, GLIS1 knockdown transcriptionally suppressed the mRNA level of the DNA methyltransferase DNMT3B, thereby attenuating HOXA9 methylation. Specifically, overexpression of DNMT3B led to DNA hypermethylation and transcriptional suppression of HOXA9, thereby partially rescuing the tumor-suppressive effects resulting from GLIS1 knockdown. Our work is the first to implicate the GLIS1/DNMT3B axis in the epigenetic silencing of HOXA9 in LUAD, highlighting the therapeutic potential of targeting GLIS1.
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高影响因子
CLINICAL & EXPERIMENTAL METASTASIS
·
2026
·Vol. 43
·期 4
·34
·
IF 3.7
Dong Chenglai,Zhu Deqi,Zhang Jincao,Gan Shaoyin,Zhao Jia,Li Chunlin,Li Bin
Metastasis contributes to treatment failure and poor prognosis of esophageal squamous cell carcinoma (ESCC) patients. The 5’-3’ exoribonuclease 2 (XRN2) is related to the pathogenesis and progression of various malignancies through its roles in transcription termination and metastasis promotion, but its function in ESCC remains unclear. Bioinformatic analysis showed that XRN2 was significantly overexpressed in ESCC tissues and was identified as a risk factor for ESCC patients. The analysis of our own cohort confirmed that XRN2 expression was overexpressed and significantly correlated with cancer stage in patients ( P = 0.0100). Gain- and loss- of function analyses revealed that XRN2 promoted ESCC cell growth, migration and invasion capabilities, as well as experimental lung colonization foci. Interestingly, we found that the RNA level of XRN2 was upregulated by the RNA-binding protein polypyrimidine tract binding protein 3 (PTBP3). Specifically, PTBP3 bound to CUUUC motifs of the 3’UTR of XRN2, prolonging the half-life of XRN2 RNA. PTBP3 was found to be significantly overexpressed in ESCC, where its expression level correlated with tumor stage ( P = 0.0164) and tumor size ( P = 0.0495), positioning it as a risk factor for ESCC patients. PTBP3 upregulation promoted ESCC cell growth, migration, and invasion in vitro and in vivo. Notably, knockdown of XRN2 reversed the tumor promotion effects induced by PTBP3 overexpression. Collectively, our data reveal a novel function of XRN2 in ESCC metastasis and the critical roles of the PTBP3/XRN2 axis in ESCC metastasis, highlighting its promise as a novel therapeutic target in ESCC. Graphical abstract
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ADVANCED FUNCTIONAL MATERIALS
·
2026
·
IF 19.9
Xinming Wang,Weichang Xie,Zichen Wang,Haonan Zhang,Jia Li,Xingjian Gao,Dingjie Zhou,Huaiyu Jiang,Shixing Huang,Qiang Zhao,Xiaofeng Ye
Repairing anisotropic tissues such as the myocardium requires implanted cells to organize into highly ordered structures. However, achieving controlled cell alignment remains a major challenge for current cell delivery patches. Here, we develop a magnetically aligned, fiber-reinforced extracellular matrix (ECM) patch that directs anisotropic cell organization and supports stem cell implantation. Poly-lactic acid fibers containing Fe 3 O 4 are fabricated via electrospinning and controlled hydrolysis, and are aligned uniaxially within ECM hydrogels using an external magnetic field prior to gelation. The resulting ECM–fiber patches exhibit enhanced mechanical strength and reliably guide the alignment of cardiomyocytes, fibroblasts, and endothelial cells. A beating patch is also created by seeding human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). In a nude mouse myocardial infarction (MI) model, implantation of iPSC-CMs@ECM–fiber patches preserves cardiac function, reduces apoptosis, limits fibrosis, and enhances vascularization. Implanted iPSC-CMs demonstrate high viability and low immunogenicity. Molecular profiling reveals transient modulation of early inflammatory responses post-MI, probably mediated through IL-17, IL-3, and IL-1β pathways. Overall, the ECM–fiber patch provides a versatile platform for delivering highly organized cells for in vivo tissue repair.
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EXPERIMENTAL EYE RESEARCH
·
2026
·
IF 3.1
Zixiang Wang,Xinyuan Yu,Yilong Shi,Yiying Chen,Zhiyang Huang,Ziyu Guo,Jianhong Zhou,Yingbin Deng
Minocycline treatment fails to ameliorate NaIO 3 - and MNU-induced retinal degeneration. • Depletion of resident retinal microglia by PLX3397 does not alleviate photoreceptor apoptosis in either model. • Clodronate liposome treatment ameliorates NaIO 3 -induced retinal pigment epithelium (RPE) toxicity. Visual impairment resulting from accidental chemical exposure is commonly encountered in emergency medicine, yet effective clinical interventions remain lacking. Given the critical roles of both resident microglia and peripheral macrophages in retinal degenerative diseases, this study systematically evaluated the protective effects of minocycline, PLX3397, and clodronate liposomes in sodium iodate (NaIO 3 )- and N-methyl-N-nitrosourea (MNU)-induced retinal degeneration models. Suppression of microglial activation with minocycline or depletion of resident microglia with PLX3397 failed to ameliorate retinal damage in either model, as evidenced by persistent fundus atrophy, diminished electroretinogram responses, and robust photoreceptor apoptosis. In contrast, systemic depletion of peripheral macrophages using clodronate liposomes significantly alleviated fundus atrophy, partially preserved visual function, and increased photoreceptor and retinal pigment epithelium (RPE) survival in the NaIO 3 model, but conferred no protection in the MNU model. These findings suggest that clodronate liposomes exert model-dependent protection, likely through modulation of peripheral macrophage-mediated RPE toxicity following chemical exposure.
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COLLOIDS AND SURFACES B-BIOINTERFACES
·
2026
·
IF 5.9
Jingting Luo,Yanyu Li,Xin Zhang,Zhen Wang,Jingjie Wang,Jia Hao,Cheng Ran,Xiaobo Ma,Zhimin Zhou
Combination therapies with two or more drugs administrated by intratympanic (IT) injection represent a promising strategy for the treatment of sensorineural hearing loss (SNHL), an inner ear disease imposing a substantial burden on patients. However, the therapeutic outcomes of conventional liquid formulations have been hindered by poor drug retention in the middle ear cavity. In the present study, a versatile hydrogel (CT Gel) was engineered for co-delivery of dexamethasone and lidocaine with drug-loaded microparticles as both cross-linkers and modular drug reservoirs. Specifically, dexamethasone microcrystals and lidocaine-loaded poly (lactic-co-glycolic acid) (PLGA) microspheres were separately prepared and subsequently coated with polydopamine (PDA). The resulting PDA-functionalized microparticles were then employed to crosslink phenylboronic acid-modified hyaluronic acid via dynamic covalent boronate ester bonds, thereby forming the hydrogel. CT Gel exhibited injectable, bioadhesive, antioxidant and sustained-release properties. Moreover, it was shown that, following IT administration in guinea pigs, CT Gel persisted in the middle ear cavity for over 7 days, enhanced drug exposure in the perilymph, and exhibited favorable biocompatibility. We anticipate that such hydrogels, crosslinked using drug-loaded microparticles as modular drug reservoirs, will find broad applications in the combinatorial treatment of inner ear disorders.
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