Directional Femoral Ultrasound-Guided Compression Technique Using in Percutaneous Mechanical Thrombectomy for Acute Deep Vein Thrombosis: A Retrospective Cohort Study.

Objective: The study aimed to investigate the early results of directional femoral ultrasound-guided compression technique (UCT) using in percutaneous mechanical thrombectomy (PMT) for acute deep vein thrombosis (DVT).

Methods: Consecutive single-center patients with acute iliofemoral DVT who underwent PMT from January 2020 to December 2021 were included. Directional femoral UCT was used to adjust the PMT catheter into the residual thrombus in the inguinal region by ultrasound compression to improve the thrombus clearance rate.

PDIA2 has a dual function in promoting androgen deprivation therapy induced venous thrombosis events and castrate resistant prostate cancer progression.

Androgen deprivation therapy (ADT) is the first line of treatment for metastatic prostate cancer (PCa) that effectively delays the tumor progression. However, it also increases the risk of venous thrombosis event (VTE) in patients, a leading cause of mortality. How a pro-thrombotic cascade is induced by ADT remains poorly understood.

Stent Graft vs Drug-Coated Balloon in Endovascular Treatment of Complex Femoropopliteal Artery Lesions: A 2-Center Experience.

Objective: Both stent grafts (SG) and drug-coated balloons (DCBs) have shown to be effective treatments for long and complex femoropopliteal (FP) lesions. However, there has not been a clinical trial comparing the 2 treatments directly. This study aims to compare the primary patency (PP) and clinical outcomes of SG and DCB for endovascular treatment of complex FP Trans-Atlantic Inter-Society Consensus (TASC) C/D lesions in patients.

Novel Self-Expanding Interwoven Nitinol Stent for Treating Femoropopliteal Artery Disease: 12-Month Results of Single-Center First-in-Man Study.

Purpose: To evaluate the safety and efficacy of Innospring stent, a novel self-expanding interwoven nitinol stent, in treating femoropopliteal atherosclerotic lesions.

Methods: A prospective, single-center, single-arm, first-in-human study enrolled 15 patients (mean age 73.1 years; 13 men) to evaluate the safety and efficacy of the Innospring stent monitored by core laboratories.

Neutrophil Extracellular Traps Delay Diabetic Wound Healing by Inducing Endothelial-to-Mesenchymal Transition via the Hippo pathway.

Diabetic foot ulcers (DFUs) are among the most frequent complications of diabetes with significant morbidity and mortality. Diabetes can trigger neutrophils to undergo histone citrullination by protein arginine deiminase 4 (encoded by in mice) and release neutrophil extracellular traps (NETs). The specific mechanism of NETs-mediated wound healing impairment in diabetes remains unknown.

CircRNA circCOL1A1 Acts as a Sponge of miR-30a-5p to Promote Vascular Smooth Cell Phenotype Switch through Regulation of Smad1 Expression.

Phenotypic switch of vascular smooth muscle cells (VSMCs) plays an important role in the pathogenesis of atherosclerosis. The mRNA expression of the synthetic biomarker Collagen Type I Alpha 1 Chain () gene is upregulated during the switch of VSMCs from the contractile to the synthetic phenotype. The association of noncoding circular RNAs transcribed by the gene with VSMC phenotype alteration and atherogenesis remains unclear.

Neutrophil extracellular traps induce abdominal aortic aneurysm formation by promoting the synthetic and proinflammatory smooth muscle cell phenotype via Hippo-YAP pathway.

The neutrophil plays an important role during abdominal aortic aneurysm (AAA) formation by undergoing histone citrullination with peptidyl arginine deiminase 4 (encoded by Padi4) and releasing neutrophil extracellular traps (NETs). However, the specific role of NETs during AAA formation is elusive. We found the levels of NET components in serum and tissues were found to be significantly associated with the clinical outcome of AAA patients.

Disulfiram accelerates diabetic foot ulcer healing by blocking NET formation via suppressing the NLRP3/Caspase-1/GSDMD pathway.

Diabetic foot ulcer (DFU) is among the most frequent complications of diabetes and is associated with significant morbidity and mortality. Excessive neutrophil extracellular traps (NETs) delay wound healing in diabetic patients. Therefore, interventions targeting NET release need to be developed to effectively prevent NET-based wound healing impairment.

Interleukin 6-regulated macrophage polarization controls atherosclerosis-associated vascular intimal hyperplasia.

Vascular intimal hyperplasia (VIH) is an important stage of atherosclerosis (AS), in which macrophages not only play a critical role in local inflammation, but also transform into foam cells to participate into plaque formation, where they appear to be heterogeneous. Recently, it was shown that CD11c+ macrophages were more associated with active plaque progression. However, the molecular regulation of phenotypic changes of plaque macrophages during VIH has not been clarified and thus addressed in the current study.

Diagnostic and Prognostic Value of Neutrophil Extracellular Trap Levels in Patients With Acute Aortic Dissection.

Background: Acute aortic dissection (AAD) is a fatal disease demanding prompt diagnosis and proper treatment. There is a lack of serum markers that can effectively assist diagnosis and predict prognosis of AAD patients.

Methods: Ninety-six AAD patients were enrolled in this study, and 249 patients with chest pain due to acute myocardial infarction, pulmonary embolism, intramural hematoma, angina or other causes and 80 healthy controls were included as control group and healthy control group.

RNA Splicing of the Abi1 Gene by MBNL1 contributes to macrophage-like phenotype modulation of vascular smooth muscle cell during atherogenesis.

Background: Vascular smooth muscle cells (VSMC) switch to macrophage-like cells after cholesterol loading, and this change may play an important role in atherogenesis. Muscleblind-like splicing regulator 1 (MBNL1) is a well-known splicing factor that has been implicated in many cellular processes. However, the role of MBNL1 in VSMC macrophage-like transdifferentiation is largely unknown.

Enhanced Autophagy in GAB1-Deficient Vascular Endothelial Cells Is Responsible for Atherosclerosis Progression.

Autophagy is a host machinery that controls cellular health. Dysfunction of autophagy is responsible for the pathogenesis of many human diseases that include atherosclerosis obliterans (ASO). Physiologically, host autophagy removes aging organelles and delays the formation of atherosclerotic plaque.

Clinical efficacy of one-stage thrombus removal via contralateral femoral and ipsilateral tibial venous access for pharmacomechanical thrombectomy in entire-limb acute deep vein thrombosis.

Objective: In the present study, we compared the early results between different approaches for pharmacomechanical thrombectomy (PMT) in the treatment of entire-limb acute deep vein thrombosis (DVT).

Methods: The present retrospective cohort study included patients with entire-limb acute DVT who had undergone PMT from January 2016 to March 2019 at two independent vascular centers. At the first center (Renji Hospital), the vascular surgeons used contralateral femoral venous access or ipsilateral tibial venous access (CFVA/ITVA).

SREBP1 suppresses the differentiation and epithelial function of hiPSC-derived endothelial cells by inhibiting the microRNA199b-5p pathway.

Human induced pluripotent stem cell (hiPSC)-derived endothelial cell (hiPSC-EC) transplantation is a promising therapy for treating peripheral artery disease (PAD). However, the poor differentiation of hiPSCs limits their clinical application. Therefore, finding key factors that regulate cellular differentiation is crucial for improving the therapeutic efficacy of hiPSC-EC transplantation.

Loss of GRB2 associated binding protein 1 in arteriosclerosis obliterans promotes host autophagy.

Background: Arteriosclerosis obliterans (ASO) is a major cause of adult limb loss worldwide. Autophagy of vascular endothelial cell (VEC) contributes to the ASO progression. However, the molecular mechanism that controls VEC autophagy remains unclear.

Mutual regulation between β-TRCP mediated REST protein degradation and Kv1.3 expression controls vascular smooth muscle cell phenotype switch.

Background And Aims: Phenotypic switch of vascular smooth muscle cells (VSMC) plays a key role in the pathogenesis of atherosclerosis and restenosis after artery intervention. Transcription repressor element 1-silencing transcription factor (REST) has been identified as key regulator of VSMC proliferation. In the present study, we sought to investigate the potential association of E3-ubiquitin ligase β-TRCP mediated REST protein degradation with Kv1.

TGFβ (Transforming Growth Factor-Beta)-Activated Kinase 1 Regulates Arteriovenous Fistula Maturation.

Objective: Arteriovenous fistulae (AVF) are the optimal conduit for hemodialysis access but have high rates of primary maturation failure. Successful AVF maturation requires wall thickening with deposition of ECM (extracellular matrix) including collagen and fibronectin, as well as lumen dilation. TAK1 (TGFβ [transforming growth factor-beta]-activated kinase 1) is a mediator of noncanonical TGFβ signaling and plays crucial roles in regulation of ECM production and deposition; therefore, we hypothesized that TAK1 regulates wall thickening and lumen dilation during AVF maturation.

Author Correction: Inhibition of the Akt1-mTORC1 Axis Alters Venous Remodeling to Improve Arteriovenous Fistula Patency.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Neutrophil Extracellular Traps Are Markers of Wound Healing Impairment in Patients with Diabetic Foot Ulcers Treated in a Multidisciplinary Setting.

Neutrophil extracellular traps (NETs) are associated with impaired wound healing in diabetes. This study evaluates the association between NET-specific markers and wound healing among diabetic foot ulcer (DFU) patients treated in a multidisciplinary setting. Clinical data of diabetic patients with active foot ulcers who presented to our team between January 1, 2016 and June 30, 2017 were recorded.

Neutrophil-Lymphocyte Ratio and Platelet-Lymphocyte Ratio Predict Severity and Prognosis of Lower Limb Arteriosclerosis Obliterans.

Background: The neutrophil-lymphocyte ratio (NLR) and platelet-lymphocyte ratio (PLR) are 2 markers of inflammation, which are associated with worse cardiovascular disease outcomes. Here, we aimed to determine the association between these ratios and disease severity and evaluate predictive validity of the NLR and PLR in lower limb arteriosclerosis obliterans (ASO).

Methods: We evaluated 211 patients with a diagnosis of ASO from January 2016 to December 2018 at Shanghai Jiaotong University Renji Hospital.

Open surgical treatment for rare epithelioid hemangioendothelioma of the common femoral vein.

Epithelioid hemangioendothelioma is a very rare disease affecting big blood vessels, especially veins. There have been very few articles describing the disease. We hereby present the case of a 56-year-old woman presenting with lower limb edema, who was initially being treated for residual thrombus in the common femoral vein but was eventually diagnosed with epithelioid hemangioendothelioma (EHE).

Inhibition of the Akt1-mTORC1 Axis Alters Venous Remodeling to Improve Arteriovenous Fistula Patency.

Arteriovenous fistulae (AVF) are the most common access created for hemodialysis, but up to 60% do not sustain dialysis within a year, suggesting a need to improve AVF maturation and patency. In a mouse AVF model, Akt1 regulates fistula wall thickness and diameter. We hypothesized that inhibition of the Akt1-mTORC1 axis alters venous remodeling to improve AVF patency.

Reduction of mitochondria and up regulation of pyruvate dehydrogenase kinase 4 of skeletal muscle in patients with chronic kidney disease.

Aim: Muscle weakness is commonly among chronic kidney disease (CKD) patients. Muscle mitochondrial dysfunction and decreased pyruvate dehydrogenase (PDH) activity occur in CKD animals but have not been confirmed in humans, and changes in pyruvate dehydrogenase kinase (PDK) and pyruvate dehydrogenase phosphatase (PDP) expression have not been evaluated in CKD muscle. We presume that the reduction of muscle mitochondria and post-translational modification of PDH may cause muscle weakness in CKD patients.

Serum miR-192 Is Related to Tubulointerstitial Lesion and Short-Term Disease Progression in IgA Nephropathy.

Background/aims: Clinical manifestation and renal histology serve as the current "gold standard" for evaluation of renal lesions in IgA nephropathy. MiR-192 is regarded as a potential noninvasive biomarker for kidney disease. We sought to elucidate a relationship between intrarenal, serum, and urinary exosomal miR-192 with renal lesions and disease progression in IgA nephropathy.