Conventional hydrogel-based vascular grafts often fail because they lack mechanical strength, and their dense structure restricts cell infiltration. To overcome these challenges, we fabricated a bilayer fabric-reinforced composite vascular graft that integrates favorable mechanical properties with biological activity. The inner layer is composed of a hydrogel matrix mixed with vascular acellular matrix (VAM) particles and sacrificial gelatin microspheres, forming an interconnected biomimetic microchannel network that serves as a "cellular highway" to guide and enhance cell migration and tissue regeneration. The outer knitted polylactic acid (PLA) mesh provides substantial mechanical strength and improves suture retention, thereby overcoming the inherent mechanical limitations of hydrogels. After implantation in a rabbit carotid artery model for 3 months, the graft remodeled into a three-layered structure resembling native vessels, demonstrating 100% patency and an effective combination of mechanical strength and biological functionality. This approach addresses key limitations of conventional hydrogel-based vascular grafts and offers a promising strategy for the development of small-diameter vascular grafts. STATEMENT OF SIGNIFICANCE: Conventional hydrogel vascular grafts are plagued by poor mechanical strength and restricted cell infiltration. We engineered a bilayer fabric-reinforced graft: its inner hydrogel-VAM matrix, embedded with sacrificial gelatin microspheres, forms interconnected microchannels as a "cellular highway" for cell migration; the outer knitted PLA mesh enhances mechanical strength and suture retention. Rabbit carotid implantation achieved 100% patency and native vessel-like three-layer remodeling at 3 months. This scalable strategy resolves the mechanical-biological trade-off, advancing vascular tissue engineering and appealing to readers focused on biomaterial clinical translation.

Cardiovascular diseases remain a leading cause of mortality worldwide, and the lack of effective small-diameter vascular grafts (SDVGs, < 6 mm) continues to limit clinical treatment options. A major challenge in the development of tissue-engineered vascular grafts (TEVGs) is the mismatch between material degradation and tissue regeneration rates, which is driven by individual variability and leads to failure in mechanical support transition, subsequent graft failure, and impeded clinical translation. Here, we report a functionally separated bilayer SDVG that decouples long-term structural support from early bioactive remodeling. The graft consists of a slowly degradable knitted polylactic acid (PLA) framework that preserves mechanical integrity, and a rapidly remodelable chitosan/gelatin (CS/GE) porous phase that promotes cell infiltration and tissue regeneration. By tuning the CS/GE composition, we identified a balanced remodeling window, in which the 1% CS/GE-PLA graft achieved favorable permeability, cytocompatibility, hemocompatibility, and mechanical performance. In a rabbit carotid interposition model, this optimized graft maintained 100% patency for 3 months and progressively remodeled into a native vessel-like trilaminar structure with endothelial coverage, smooth muscle organization, and extracellular matrix maturation. This bilayer design provides a strategy to coordinate scaffold degradation with tissue regeneration, enabling stable mechanical support and functional vascular remodeling in small-diameter grafts.

Arteriovenous fistulas (AVFs) are preferred access points for hemodialysis. The present study aimed to investigate the function of early growth response‑1 (Egr‑1) in the proliferation and migration of smooth muscle cells (SMCs) and assess its potential as a new therapeutic target for AVF treatment. A comprehensive analysis combining public data‑source mining, human tissue collection, animal studies, cell culture experiments and various molecular biology techniques was conducted. The public dataset GSE119296 was used for immunohistochemical analyses of human AVF stenosis samples. SMC‑specific Egr‑1 knockout mice and various in vitro assays on primary rat vascular SMCs were used to evaluate the effect of Egr‑1 on the functional capacity of SMCs. RNA sequencing and chromatin immunoprecipitation sequencing was performed. Egr‑1 was upregulated in human AVF stenosis samples and cultured SMCs. Knockout of Egr‑1 in mice mitigated AVF outflow tract stenosis, improved flow dynamics and diminished neointima formation. In vitro, Egr‑1 ablation reduced SMC proliferation and migration; Egr‑1 transcriptionally activated Egr‑2. Increased Egr‑1 expression facilitated SMC proliferation and migration through Egr‑2 regulation, contributing to AVF stenosis. Consequently, targeting Egr‑1 may offer a novel therapeutic approach for managing AVF intimal hyperplasia and improving AVF patency and function in patients with end‑stage renal disease.

The frequent failures of small-diameter vascular grafts (SDVGs) mainly result from thrombosis and insufficient endothelialization. Despite recent biochemical modification strategies aiming to enhance long-term patency, the challenges of suppressing thrombosis and promoting rapid endothelialization persist. We thus designed a biomimetic three-layer flexible vascular graft scaffold. This scaffold precisely replicates the nonlinear mechanical responses of vascular tissues and promotes vascular regeneration by minimizing the mechanical mismatch between the graft and the host. The biomimetic flexible SDVG scaffold comprises a screwed inner layer, a middle fabric layer, and a Polyethylene terephthalate (PET) helical coil. It shows excellent bending resistance and resilience, reducing thrombosis formation caused by impaired blood flow during bending. Moreover, this scaffold notably improves the adhesion, spreading, proliferation, and elongation of endothelial cells, facilitating luminal remodeling and maintaining long-term patency through its intimal topography. In vivo studies demonstrate that the endothelial layer forms within three months of implantation, ensuring long-term patency. By three months after implantation, both the endothelial and smooth muscle layers are regenerated, developing hierarchical microstructures and compositions similar to those of native vessels. The biomimetic flexible vascular graft with screwed structures exhibits excellent bending resistance and enhanced vascular remodeling, thereby promoting blood vessel regeneration and showing strong potential for clinical translation.

(1) Background: Arteriovenous fistulas (AVFs) are the preferred site for hemodialysis. Unfortunately, approximately 60% of patients suffer from AVF failure within one year. Oxidative stress plays an important role in the occurrence and development of AVF. However, the underlying mechanisms remain unclear. Therefore, specific oxidative stress-related biomarkers are urgently needed for the diagnosis and treatment of AVF failure. (2) Methods: Bioinformatics analysis was carried out on dataset GSE119296 to screen for PTGS2 as a candidate gene related to oxidative stress and to verify the expression level and diagnostic efficacy of PTGS2 in clinical patients. The effects of NS398, a PTGS2 inhibitor, on hemodynamics, smooth muscle cell proliferation, migration, and oxidative stress were evaluated in a mouse AVF model. (3) Results: Based on 83 oxidative stress-related differentially expressed genes, we identified the important pathways related to oxidative stress. PTGS2 may have diagnostic and therapeutic efficacy for AVF failure. We further confirmed this finding using clinical specimens and validation datasets. The animal experiments illustrated that NS398 administration could reduce neointimal area (average decrease: 49%) and improve peak velocity (average increase: 53%). (4) Conclusions: Our study identified PTGS2 as an important oxidative stress-related biomarker for AVF failure. Targeting PTGS2 reduced oxidative stress and improved hemodynamics in an AVF mouse model.

Acute pulmonary embolism (APE) has a high mortality rate worldwide. The cause of death from pulmonary embolism (PE) is predominantly progressive right heart failure, which is common in intermediate-high-risk and high-risk patients. The latest guidelines recommend reperfusion thrombolytic therapy for high-risk patients, but it is rarely practiced clinically, given the high rate of intracranial hemorrhage. Moreover, the optimal treatment for intermediate-risk patients remains undetermined. With the development of technology, a series of endovascular interventional treatments are widely used in patients with intermediate-high-risk or high-risk PE, such as standard catheter-directed thrombolysis (SCDT), ultrasound-assisted thrombolysis (USAT), pharmacomechanical catheter-directed thrombolysis (PM-CDT) and mechanical thrombectomy (MT). Current studies have shown that interventional therapy can effectively improve right heart function and reduce the incidence of cerebral hemorrhage. Future research should mainly focus on screening patients who benefit from interventional therapy, reducing mortality, and improving long-term sequelae. This article aimed to review these treatment devices and provide an update on the research progress related to interventional therapy for PE. In addition, we introduce a risk stratification assessment for APE in the updated guidelines and provide an overview of risk indicators and APE scores for judging prognosis. Finally, we discuss the long-term outcomes of APE in combination with interventional therapy.

Arteriovenous fistulas (AVFs) have long been used as dialysis access in patients with end-stage renal disease; however, their maturation and long-term patency still fall short of clinical needs. Rodent models are irreplaceable to facilitate the study of mechanisms and provide reliable insights into clinical problems. The ideal rodent AVF model recapitulates the major features and pathology of human disease as closely as possible, and pre-induction of the uremic milieu is an important addition to AVF failure studies. Herein, we review different surgical methods used so far to create AVF in rodents, including surgical suturing, needle puncture, and the cuff technique. We also summarize commonly used evaluations after AVF placement. The aim was to provide recent advances and ideas for better selection and induction of rodent AVF models. At the same time, further improvements in the models and a deeper understanding of AVF failure mechanisms are expected.

(1) Background: Arteriovenous fistulas (AVFs) are the preferred access for hemodialysis. Unfortunately, about 60% of patients, especially female patients, fail to receive normal dialysis within one year after surgery because of AVF failure. However, the underlying mechanisms caused by sex differences in AVF failure remain unclear. (2) Methods: We performed analysis of DEGs and functional analysis with the dataset GSE119296 to reveal the biology underlying AVF failure. Immune responses were calculated using CIBERSORT. A protein–protein interaction network and hub gene were constructed using STRING and stepwise identification of potential drugs was performed online. (3) Results: Functional analysis showed that extracellular matrix reprogramming and PI3K-AKT pathway enrichment were significant in both male and female patients. COL1A1 was the hub gene in male patients, whereas CDK1 was the hub gene in female patients. Immune responses including γδ-T cells and mast cells are activated in female patients while no significant differences were noted in the male group. (4) Conclusions: In this study, we used a series of mature and recognized bioinformatic strategies to determine the following items: (1) Reveal the pathogenesis of AVF failure through HUB genes and signaling pathways between the different sexes. (2) Determine the relationship between sex differences in AVF failure and immune abnormalities. (3) Search for relevant sex-specific drugs targeting AVF failure.

Abstract Background Although there is considerable evidence suggesting a link between gut microbiota (GM) composition and venous thromboembolism (VTE)/deep vein thrombosis (DVT)/pulmonary embolism (PE), population-level studies that can establish a causal relationship are currently lacking. Methods Using two-sample Mendelian randomization (MR) approach was used to examine the causal effects of 211 GM and 489 plasma metabolites on VTE/PE/DVT. We employed instrumental variables comprised of single nucleotide polymorphisms (SNPs) strongly associated with GM composition and plasma metabolite levels to determine whether these factors play a causal role in the development of VTE/DVT/PE. Additionally, we conducted mediation analysis to explore the potential associations between specific taxonomic groups and metabolites. Results The MR analysis revealed significant associations between 16 taxonomic units and 40 metabolites with VTE/DVT/PE as the causative factors. Among these, Firmicutes, Clostridia, Roseburia, Ruminococcaceae NK4A214, and Intestinimonas were found to have a protective effect against VTE/DVT/PE. In contrast, Bacteroidetes, Anaerotruncus, Victivallales, Desulfovibrionaceae, Clostridium innocuum, Eubacterium oxidoreducens, and Lachnoclostridium have been identified as risk factors for VTE/DVT/PE. Reverse MR analysis revealed 11 associations between VTE/DVT/PE and GM. Furthermore, no significant heterogeneity or horizontal pleiotropy was observed in any of the instrumental variables. Mediation analysis revealed 10 intermediate relationships, and metabolic pathway analysis identified 6 significant pathways. Conclusions Our study emphasizes the significant causal associations between the gut microbiota (GM), plasma metabolome, and VTE/DVT/PE. These interconnections have the potential to be used as clinical biomarkers for risk stratification and prognosis assessment in patients with VTE/DVT/PE.

Background:Aortic dissection (AD) poses a great threat to the life of patients; however, there is currently no documentation of a clear pathogenic mechanism of this disease. In recent years, β-aminopropionitrile (BAPN)-induced AD in rodents has been widely used in basic research, which provides a good platform for exploring the pathogenesis of AD and drug modification. This study aimed to identify molecular markers and pathways for the diagnosis and treatment of AD by comparing a murine AD model and human AD transcriptome through a bioinformatics analysis.Methods:We constructed a BAPN-induced mice model and performed high-throughput sequencing analysis. The GSE147026 dataset of patients was obtained from the Gene Expression Omnibus database. We performed a subsequent bioinformatics analysis of human AD and the murine AD model using R software. The DESeq software package was used to analyze the differentially expressed genes (DEGs). Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed to analyze the enrichment pathways. Protein-protein interaction network construction and hub gene selection were based on STRING software analysis. Stepwise identification of potential drugs was performed online, while hub genes were validated immunohistochemically.Results:We compared the murine AD model and human AD transcriptome and found that both differentially expressed 463 genes. The cytokine-cytokine receptor interaction, tuberculosis, and phagosome pathways were significantly enriched. CDC20, CCNB2, and CCNB1 may be associated with AD development. Protein-drug interactions were also identified.Conclusions:This study is the first to reveal transcriptional changes in a murine BAPN-induced AD model versus human AD transcriptome. Furthermore, we identified the important hub genes, related pathways, and potential drugs by analyzing the overlapping DEGs between human AD and the murine AD model. Our results provide a basis for the further identification of potential molecular markers for diagnosing and treating AD.

This is a rare fatty abdominal aortic aneurysm (AAA) in a man in his 52s (Panels A–D). The patient presented with a 1 year history of pulsatile mass and intermittent abdominal distension. He had a 5-year medical history of hypertension which was well controlled by daily Irbesartan therapy (75 mg, po, qd). Examination revealed one pulsatile mass was touchable in the middle quadrant. The D-dimer test result was 8.32 mg/L (normal <0.5). An abdominal ultrasound Doppler showed that the infrarenal aorta was dilated to as big as 67 × 59 mm accompanying with hypoechoic attachment in the inner side of the dilated aorta. Next, a routine aortic computed tomographic angiography (CTA) was performed, and CTA determined this pulsatile mass as AAA. We admitted his presumed diagnosis as AAA with intraluminal thrombus (ILT). Considering his therapeutic willingness, we performed an open surgery for this patient. However, after dissection of the AAA mass, we found plenty of lipoid lesions in the vessel wall—with no evidence of ILT (Panels E–H). Postoperative histological and dual energy computed tomography (CT) scan analysis presented that there was extensive oil red (+) staining in the vessel wall (Panels I–Q).

Cardiovascular diseases (CVDs) are still a major cause of global mortality and disability, seriously affecting people’s lives. Due to the severity and complexity of these diseases, it is important to find new regulatory mechanisms to treat CVDs. Ferroptosis is a new kind of regulatory cell death currently being investigated. Increasing evidence showed that ferroptosis plays an important role in CVDs, such as in ischemia/reperfusion injury, heart failure, cardiomyopathy, and atherosclerosis. Protecting against CVDs by targeting ferroptosis is a promising approach; therefore, in this review, we summarized the latest regulatory mechanism of ferroptosis and the current studies related to each CVD, followed by critical perspectives on the ferroptotic treatment of CVDs and the future direction of this intriguing biology.

Background: Coronavirus disease 2019 (COVID-19) has become a global pandemic which may compromise the management of vascular emergencies. An uncompromised treatment for ruptured abdominal aortic aneurysm (rAAA) during such a health crisis represents a challenge. This study aimed to demonstrate the treatment outcomes of rAAA and the perioperative prevention of cross-infection under the COVID-19 pandemic.

Cardiovascular disease serves as the leading cause of death worldwide, with stenosis, occlusion, or severe dysfunction of blood vessels being its pathophysiological mechanism. Vascular replacement is the preferred surgical option for treating obstructed vascular structures. Due to the limited availability of healthy autologous vessels as well as the incidence of postoperative complications, there is an increasing demand for artificial blood vessels. From synthetic to natural, or a mixture of these components, numerous materials have been used to prepare artificial vascular grafts. Although synthetic grafts are more appropriate for use in medium to large-diameter vessels, they fail when replacing small-diameter vessels. Tissue-engineered vascular grafts are very likely to be an ideal alternative to autologous grafts in small-diameter vessels and are worthy of further investigation. However, a multitude of problems remain that must be resolved before they can be used in biomedical applications. Accordingly, this review attempts to describe these problems and provide a discussion of the generation of artificial blood vessels. In addition, we deliberate on current state-of-the-art technologies for creating artificial blood vessels, including advances in materials, fabrication techniques, various methods of surface modification, as well as preclinical and clinical applications. Furthermore, the evaluation of grafts both in vivo and in vitro, mechanical properties, challenges, and directions for further research are also discussed.

Recent advances in the pathophysiologic understanding of coronavirus disease 2019 (COVID-19) suggests that cytokine release syndrome (CRS) has an association with the severity of disease, which is characterized by increased tumor necrosis factor α (TNF-α), interleukin (IL)-6, IL-2, IL-7, and IL-10. Hence, managing CRS has been recommended for rescuing severe COVID-19 patients. TNF-α, one of the pro-inflammatory cytokines commonly upregulated in acute lung injury, triggers CRS and facilitates SARS-CoV-2 interaction with angiotensin-converting enzyme 2 (ACE2). TNF-α inhibitors, therefore, may serve as an effective therapeutic strategy for attenuating disease progression in severe SARS-CoV-2 infection. Below, we review the possibilities and challenges of targeting the TNF-α pathway in COVID-19 treatment.

For more than half a century, arteriovenous fistula (AVFs) has been recognized as a lifeline for patients requiring hemodialysis (HD). With its higher long-term patency rate and lower probability of complications, AVF is strongly recommended by guidelines in different areas as the first choice for vascular access for HD patients, and its proportion of application is gradually increasing. Despite technological improvements and advances in the standards of postoperative care, many deficiencies are still encountered in the use of AVF related to its high incidence of failure due to unsuccessful maturation to adequately support HD and the development of neointimal hyperplasia (NIH), which narrows the AVF lumen. AVF failure is linked to the activation and migration of vascular cells and the remodeling of the extracellular matrix, where complex interactions between cytokines, adhesion molecules, and inflammatory mediators lead to poor adaptive remodeling. Oxidative stress also plays a vital role in AVF failure, and a growing amount of data suggest a link between AVF failure and oxidative stress. In this review, we summarize the present understanding of the pathophysiology of AVF failure. Furthermore, we focus on the relation between oxidative stress and AVF dysfunction. Finally, we discuss potential therapies for addressing AVF failure based on targeting oxidative stress.

急性复杂性Stanford B型主动脉夹层是一种隐匿性强且致死率高的临床急症,并发症常有主动脉破裂或主动脉重要分支严重缺如等.急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)是肺实质细胞损伤而导致,主要表现为急性呼吸窘迫及顽固性低氧血症的临床综合征,极易被误诊及漏诊,致死率高.目前对Stanford B型主动脉夹层并发ARDS研究报道较少,华中科技大学同济医学院附属协和医院收治1例急性Stanford B型主动脉夹层患者,在手术前连续两次发生重症ARDS,但通过高级生命支持及对症治疗后生命体征稳定,并在术后1年和5年复查显示恢复良好.本研究通过探讨急性Stanford B型夹层合并ARDS的发病机制、手术治疗及预防进行文献回顾,现报道如下.

目的 比较机械血栓抽吸术和置管溶栓术治疗急性下肢深静脉血栓的有效性和安全性.方法 选取我院血管外科2018年2月～2019年2月的下肢深静脉血栓病人80例,根据治疗方案不同分为机械血栓抽吸组和置管溶栓组.分析两组静脉通畅率、D-二聚体、并发症、尿激酶总使用量以及住院时间.结果 机械血栓抽吸组和置管溶栓组的术后静脉通畅评分分别为(1.90±1.02)和(2.16±1.10),静脉通畅率分别为(85.84±11.48)％和(84.40±14.71)％,住院总时间分别为(13.57±4.76)天和(12.98±4.55)天,治疗期间均出现少量不同程度各类并发症(包括出血、感染、过敏等),两组比较差异无统计学意义(P＞0.05).两组D-二聚体降至正常值时间分别为(6.30±1.23)天和(8.2±1.59)天,尿激酶总使用量分别为(22.6±3.4)万单位和(278.4±103.5)万单位,住院总费用分别为(9.4±3.1)万和(4.7±2.3)万,两组比较差异有统计学意义(P＜0.05).结论 机械血栓抽吸术及置管溶栓术在围术期均体现出良好的安全性,均能短时间内有效清除血栓,机械血栓抽吸术组住院时间短、溶栓药物使用更少、D-二聚体下降更快,但费用增加.

The coronavirus disease 2019 (COVID-19) can cause venous thromboembolism, including deep venous thrombosis (DVT) and pulmonary embolism (PE), but there has been little research on the implantation of an inferior vena cava filter (IVCF) to prevent lethal PE complications. The purpose of this study is to determine the feasibility and effectiveness of IVCF implantation in DVT-COVID-19 patients through the aid of X-ray and bedside color ultrasound (US) techniques. We present three COVID-19 cases that were simultaneously confirmed as acute DVT. The first DVT-COVID-19 patient suffered from unexpected hemiplegia in the right limb. Due to the possibility of a cerebral hemorrhage, we performed X-ray-guided IVCF insertion to prevent PE occurrence. The second patient was diagnosed as having right limb gangrene. Due to the severe infection, we performed one bedside US-guided IVCF implantation before his acute right thigh amputation on the same day. The third patient complained of a feeling of paralysis in his left lower extremity. The X-ray radiograph determined thoracic and lumbar vertebra fractures. We also performed one bedside US-guided IVCF implantation before his vertebra internal fixation surgery. After the standard treatments, the first and third patients were discharged, while the second patient died due to an unexpected acute cardiovascular disease event in the intensive care unit. US-guided IVCF implantation is an effective method that can be considered as a precautionary strategy for preventing lethal PE occurrence, especially for critical DVT-COVID-19 patients who are not suitable to be transferred to a routine X-ray operation room.

目的 探讨经皮机械性血栓切除术(PMT)与置管溶栓术(CDT)在防治血栓形成后综合征(PTS)中的作用.方法 收集2018年2月至2019年2月华中科技大学同济医学院附属协和医院收治的80例患者的临床资料,按照治疗方法的不同将其分为PMT组和CDT组,每组40例.PMT组行AngioJet血栓抽吸术,CDT组行CDT.比较两组患者的小腿腿围缩小情况、消肿率、小腿腿围缩小时间及PTS的发生率.结果 对健侧与患侧小腿踝部腿围周径差值、小腿最粗段腿围周径差值和膝下15 cm腿围周径差值行重复测量方差分析,结果显示,两组患者不同时间点(术前1 d及术后2、4、6 d)的差值比较,差异均有统计学意义(P时间<0.01);两组患者组间差值比较,差异均无统计学意义(P组间>0.05);两组患者的差值在组间·时间点间比较,差异均有统计学意义(P交互<0.01).术后1周,PMT组患者下肢不同节段的消肿率高于CDT组患者(P<0.05).PMT组小腿最粗段健侧与患侧腿围差值缩小50％的所需时间短于CDT组(P<0.01).随访期间,两组的PTS发生情况比较,差异无统计学意义(P>0.05).结论 PMT与CDT相比,消除下肢肿胀具有一定的优势,可能为DVT患者血栓清除策略提供更优的选择.