Anatomical and microscopic evaluation of the liver in migratory shoveler ducks (Spatula clypeata): A multi-modal study using gross anatomy, vascular casting, morphometric analysis, and histochemistry techniques.

Lacrimal gland spheroids in tissue specific hydrogel for dry eye modelling.

A β-Si3N4/HA composite materials with biomimetic mineralized CaCO3 coating promote angiogenesis and bone regeneration through immunomodulation.

Oroxindin promotes angiogenesis in pressure ulcers through activating PI3K/AKT signaling pathway by PTEN suppression.

Ethyl ferulate suppresses choroidal neovascularization by accelerating Keap1 degradation through the inhibition of PSMD14-mediated deubiquitination.

Targeting PFKFB3-dependent endothelial-mesenchymal transition by luteolin attenuates doxorubicin-induced cardiotoxicity.

Impinging flow regulates endothelial cell injury via HMGB1-mediated ferroptosis to promote intracranial aneurysm formation and progression.

Homoplantaginin alleviates high glucose-induced vascular endothelial barrier dysfunction by regulating Yes-associated protein 1.

Functional iron oxide nanoparticles cross-linked hydrogel for craniofacial bone regeneration.

Sustainable MXene-based wearable sensor reinforced with microcrystalline cellulose for human motion monitoring in subzero environments with integrated machine learning.

Effects of the Dental Implant Surface Topography and Macrophage Polarisation on Osteogenesis and Angiogenesis.

Abdominal wall defects caused by trauma, tumors, infections, abdominal surgery, and congenital factors can lead to functional impairments. The use of patches remains the most effective treatment approach. However, current repair materials still have limitations in regulating inflammation and promoting vascularization. Here, a small intestinal submucosa (SIS) extracellular patch was developed via conjugation with functional peptides PR1P and LL37 (i.e., SIS-PR1P-LL37), to achieve angiogenesis and inflammation modulation for abdominal wall repair. In vitro experiments confirmed its superior pro-angiogenic potential when human umbilical vein endothelial cells (HUVECs) were treated with the patch, both tube formation (total tube length: 4.51 ± 0.53mm, junction count: 28.00 ± 4.97) and scratch wound repair (repair area 3.26-fold that of the SIS group) outperformed the native SIS group (average tube length: ∼1.3mm). After 7 days of culture, the VEGF expression was higher than that in the SIS group, and the expression levels of key angiogenic genes (VEGF, VEGFR-2, etc.) were 5.45-7.82-fold higher than those in the control group. Additionally, this peptide-conjugated SIS patch could enhance cell proliferation and angiogenic differentiation, effectively reduce the levels of inflammatory cytokines, and enrich the TLR and VEGF signaling pathways. The rat abdominal wall defect model further confirmed its superior capacity for tissue regeneration and angiogenesis, indicating it provides important theoretical and experimental support for the development of novel bioactive patches and holding promise for optimizing clinical strategies for abdominal wall repair.

The present study investigated the combined effects of zofenoprilat (ZOFE) and nebivolol (NEBI) on endothelial function, focusing on their anti-inflammatory and antioxidant properties. The purpose was to evaluate whether these drugs, commonly used in clinical practice, offer a synergistic therapeutic strategy for managing hypertension and protecting vascular health. ZOFE, an ACE inhibitor, demonstrated significant anti-inflammatory activities by reducing inflammatory cytokines, thereby mitigating vascular inflammation, a key factor in hypertension and atherosclerosis. NEBI, a third-generation beta-blocker, exhibited strong antioxidant effects by enhancing nitric oxide (NO) levels, crucial for maintaining endothelial function and reducing oxidative stress. The potential effect of ZOFE and NEBI treatment was evaluated using human umbilical vein endothelial cells (HUVEC) as a model. Specifically, cells were challenged with tumor necrosis factor-α (TNF-α) to induce endothelial dysfunction. Subsequently, cell viability, NO production, protein levels of superoxide dismutase (SOD) and catalase (CAT), enzymatic activity of SOD and CAT, intracellular levels of glutathione (GSH), inflammatory status, and levels of interleukin-6 (IL-6) monocyte chemoattractant protein-1 (MCP-1), macrophage inhibitory cytokine-1 (MIC-1), and the active form of nuclear factor kappa B (p-NFκB), were analyzed. Our results showed that NEBI significantly counteracted oxidative stress, increasing the main antioxidant defenses (SOD, CAT, and GSH). The combination of ZOFE and NEBI resulted in a potentiated effect, enhancing both anti-inflammatory and antioxidant activities. This dual mechanism of action provides a comprehensive approach to protecting endothelial cells and improving vascular function. The combined therapy not only lowered blood pressure more effectively but also offered greater protection against endothelial damage compared to monotherapy with either drug alone. These findings suggest that the combination of ZOFE and NEBI could be particularly beneficial for patients with hypertension, especially those with coexisting inflammatory and oxidative stress-related conditions. This combination therapy, by addressing multiple pathogenic pathways simultaneously, could potentially be beneficial in patients with cardiovascular risk conditions. In conclusion, the combination of ZOFE and NEBI offers a potentially promising therapeutic approach for managing hypertension and protecting vascular health, aiming at improving clinical outcomes for patients with cardiovascular diseases. Not applicable.

Substitution-degree-engineered acetylated curdlan Janus dressing: Unidirectional self-pumping for efficient wound exudate management and accelerated healing.

Ovarian cancer is one of the most prevalent gynecologic malignancies worldwide. Dysregulated cell proliferation and angiogenesis are well-recognized to be involved in the pathogenesis of ovarian cancer. Nucleolar Protein 7 (NOL7), a novel RNA-binding protein, has been identified as a tumor suppressor and a key anti-angiogenetic factor. However, the function of NOL7 and its underlying molecular mechanisms in ovarian cancer remain unclear. In this study, we demonstrated that NOL7 expression was down-regulated in ovarian cancer tissues, and low NOL7 expression was associated with poorer prognosis in patients with ovarian cancer. Overexpression of NOL7 decreased cell viability, inhibited cell cycle entry and proliferation, and promoted apoptosis in OVCAR-3 and SKOV-3 cells. Additionally, NOL7 overexpression decreased VEGF-A level, increased TSP-1, and suppressed angiogenesis of human umbilical vein endothelial cells (HUVECs). Conversely, knockdown of NOL7 in ovarian cancer cells enhanced cell proliferation and angiogenesis, while reducing apoptosis. Invivo experiments further confirmed that NOL7 overexpression inhibited tumor growth and angiogenesis. Mechanistic studies revealed that NOL7 could bind to the 3'UTR of growth arrest and DNA damage inducible alpha (GADD45A), and overexpression of NOL7 up-regulated GADD45A expression by stabilizing GADD45A mRNA in ovarian cancer cells. The anti-cancer effects of the NOL7/GADD45A were mediated by inhibiting the phosphorylation of STAT3 at Ser727. Collectively, our findings indicate that NOL7 functions as a tumor suppressor in ovarian cancer and provide a novel therapeutic target for the treatment of ovarian cancer.

Chronic kidney disease (CKD) is characterized not only by progressive fibrosis but also by systemic endothelial dysfunction and inflammation. Platelets, traditionally recognized for their role in hemostasis, also serve as key modulators of endothelial activation and immune cell recruitment. Platelet activation is commonly observed in patients with CKD and contributes to the proinflammatory environment. Although platelet-endothelial interactions are well-characterized in cardiovascular disease, their role in renal endothelial dysfunction and inflammation remains poorly understood. To investigate this, we used the unilateral ureteral obstruction (UUO) model in mice, to examine how platelet activation influences endothelial responses and monocyte/macrophage recruitment in the early phase of renal fibrosis development. Platelet depletion reduced the number of infiltrating macrophages in kidney tissue, decreased expression of endothelial activation and inflammation markers, and preserved the peritubular capillary (PTC) integrity. Further in vitro studies using human umbilical vein endothelial cells (HUVECs) showed that activated platelets induced endothelial dysfunction and inflammation, in line with the in vivo findings. To recapitulate the vascular microenvironment, we performed a shear flow-based transmigration assay. Monocyte adhesion and transendothelial migration significantly increased when endothelial cells were pretreated with activated platelets compared to unstimulated controls. Moreover, the presence of platelets on the inflamed endothelium further enhanced monocyte migration, suggesting a synergistic effect in promoting immune cell recruitment. Collectively, our findings highlight that activated platelets contribute to endothelial dysfunction, inflammation, and monocyte infiltration in early kidney injury, suggesting their potential as a therapeutic target to mitigate microvascular injury and preserve renal vascular integrity in kidney disease.

Complete congenital atrioventricular heart block (CHB) is a rare but serious, life-threatening condition in neonates, most often associated with maternal autoimmune connective tissue disease. Definitive management typically requires epicardial pacing; however, in cases of life-threatening bradycardia and hemodynamic compromise, temporary transvenous pacing may be lifesaving. Securing vascular access in premature or low-birth-weight infants often makes vascular access technically challenging, and conventional routes may not always be feasible. In such situations, the umbilical vein offers a rapid, bedside, and less invasive alternative. We present the case of a premature neonate born at 35 + 1 weeks with congenital third-degree heart block, in whom emergency temporary pacing was successfully performed via the umbilical vein after failed femoral access, subsequently serving as a bridge to permanent pacemaker implantation.

Sodium Danshensu (SDSS) shows potential in treating diabetic wounds (DWs) owing to its antioxidant, anti-inflammatory, and pro-angiogenesis effects. The specific pharmacological mechanisms of SDSS in achieving the above effects were evaluated. The potential targets of SDSS and DWs were obtained from online databases. Interaction networks were constructed using network pharmacology, and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed. Combined with machine learning, the biological targets were evaluated and prioritized. A high-glucose-induced human umbilical vein endothelial cell (HUVEC) model was established for in vitro studies. A total of 126 shared targets of SDSS and DWs were selected, and the core targets included EGFR, CASP3, SRC, ESR1, JUN, NFKB1, IGF1R, ESR2, AR, and PPARG. KEGG enrichment analysis revealed significant enrichment of the PI3K-AKT signaling pathway (P < 0.05). Machine learning indicated EGFR as a key target of SDSS in treating DWs. Findings from molecular docking and molecular dynamics simulation confirmed the stable combination of SDSS and EGFR. In vitro experiments indicated that SDSS may activate the PI3K-AKT pathway via EGFR targets, improve the mobility of high-glucose-induced HUVECs, and increase lumen formation (branch number). It promoted catalase production and inhibited the release of malondialdehyde and inflammatory factors including tumor necrosis factor-α and interleukin-6 (all P < 0.05). SDSS activates the PI3K-AKT pathway via EGFR, promotes endothelial cell migration and angiogenesis, and inhibits oxidative stress and the inflammatory response, highlighting its potential in treating DWs.

pathological angiogenesis is a critical driver of hypertrophic scar (HS) formation, a common fibrotic skin disorder with limited therapeutic options. However, the precise molecular pathways governing scar-associated neovascularization remain incompletely understood. This study aims to develop a biomaterial-based targeted delivery system to inhibit angiogenesis-driven HS progression. An in vitro scar angiogenesis model was established by culturing human umbilical vein endothelial cells (HUVECs) with HS fibroblast-conditioned medium (HSCM). Transcriptomic analysis was performed using RNA sequencing, followed by KEGG pathway analysis. The effects of the ERK inhibitor SCH772984 and of targeted MAP2K1 knockdown on HUVECs proliferation were assessed. For in vivo validation, a dissolvable microneedle arrays (DMNAs) made from methacrylate hyaluronic acid (HAMA) was loaded with SCH772984 and applied to a rabbit ear model of HS. Statistical analyses were conducted using Student's t-test and one-way ANOVA, with P < 0.05 considered significant. Transcriptomic analysis of the in vitro model revealed significant upregulation of the MAPK, mTOR, and PI3K-Akt signaling pathways. Pharmacological inhibition of ERK with SCH772984 suppressed endothelial cell proliferation. Mechanistically, this effect was phenocopied by targeted knockdown of MAP2K1, confirming the central role of the MAP2K1/ERK signaling axis in promoting scar angiogenesis. In the rabbit ear model, treatment with SCH772984-loaded DMNAs significantly reduced the scar elevation index (SEI) and downregulated markers of both myofibroblast activation and neovascularization compared to control groups. This study highlights the critical role of the MAP2K1/ERK pathway in mediating HS angiogenesis. Furthermore, the SCH772984-loaded DMNA platform described here is a promising and minimally invasive transdermal therapeutic approach for the clinical management of HS.

Polygonum capitatum (PC), known as “Tou Hua Liao” (Chinese name), is an essential source of Hmong medicinal plants, which has been used for treating various human diseases. This study examined whether PC has lipid-lowering and anti-atherosclerotic effects and explored the underlying mechanisms. We focused on PC’s influence on gut microbiota–derived metabolites. First, we analyzed animal-derived serum containing PC components and the botanical compounds of PC by UPLC-MS/MS to identify potential bioactive constituents. Second, we treated high-fat diet–fed hamsters with PC to determine whether the treatment improved plasma lipids and attenuated atherosclerosis progression. We then assessed PC’s effects on the gut microbiota by 16S rDNA sequencing and performed fecal microbiota transplantation in hamster models. Finally, we used human umbilical vein endothelial cells (HUVECs) to probe molecular mechanisms by which PC might inhibit oxidative stress and apoptosis. In a diet-induced atherosclerotic hamster model, PC treatment reduced atherosclerosis by decreasing lipid accumulation, oxidative stress, and apoptosis, and it restored gut microbiota balance while markedly lowering the abundance of TMAO-producing bacteria. PC also exerted antioxidant and anti-apoptotic effects and inhibited endothelial apoptosis via an MCPIP1-dependent mechanism. Together, these results indicate that PC suppresses atherosclerosis through two likely pathways: reduction of gut microbiota–derived TMAO production and inhibition of oxidative stress–driven endothelial apoptosis. Network pharmacology analysis of PC-specific blood-absorbed components supports these findings.Supplementary InformationThe online version contains supplementary material available at 10.1186/s13020-026-01355-7.