Background: Exosome (Exo) secreted by bone mesenchymal stem cells (BMSCs) enhances cutaneous wound healing in mouse with diabetes mellitus (DM). However, the mechanism remains unclear. Methods: Next-generation sequencing (NGS) was applied to study abnormal circular RNA (circRNA) expressions in ulcer tissues with or without Exo treatment. Bioinformatics and luciferase outputs were employed to verify interactional correlations amongst RNAs. EPCs cells were utilized to study the ROS under high glucose conditions by immunofluorescence. A DM ulceration mouse model was established and the therapeutic Exo effect was investigated through immunofluorescence. Results: Data showcased that Exo treatment significantly promoted cutaneous wound healing in mice with DM. NGS discovered that circ-Snhg11 functioned in Exo-mediated tissues repair. circ-Snhg11 downregulation reduced therapeutic effects regarding Exo upon wound healing in diabetic mice. Bioinformatics and luciferase reporting outcomes verified that both miR-144-3p and SLC7A11 were circ-Snhg11 downstream targets. SLC7A11 downregulation or miR-144-3p overexpression reversed protective effect regarding circ-Snhg11 on EPCs after exposure to a high glucose microenvironment. circ-Snhg11 upregulation increased the therapeutic Exo effect on wound healing in diabetic mice by stimulating angiogenesis and reducing GPX4-mediated ferroptosis. Furthermore, Exo circ-Snhg11 delivery promoted the miR-144-3p/SLC7A11/GPX4 signal. Conclusions: In conclusion, circ-Snhg11 from BMSC Exo promoted the SLC7A11/GPX4-mediated anti-ferroptosis signal by sponging miR-144-3p. This promoted angiopoiesis and accelerated diabetic wound healing.

Venous thromboembolism (VTE) refers to deep venous thrombosis (DVT) and pulmonary embolism (PE), which is a worldwide problem and has very high morbidity and mortality. The research of venous thrombosis involves pathogenesis, pathophysiology, and therapeutic attempt. Alternative experimental animal models have changed dramatically over the past 20 years, from small murine models to large ones. Larger animal models offer more options and are more consistent with human physiology. This article aims to induce chronic deep venous thrombosis in the left iliac vein in canine and porcine models and compare these two models. We think that feasible large animal models can better translate the results of therapeutic research into clinical application.

Acute lower limb ischemia (ALI) with antiphospholipid syndrome (APS) is a potentially fatal disease. We performed retrospective analysis of prospectively collected data from patients examined from January 2015 to January 2021 that were diagnosed with definite APS and ALI, and tested positive for antiphospholipid antibodies; had undergone computed tomographic angiography or color doppler ultrasound, and showed clinical manifestations. In total, 72 APS-ALI patients were enrolled in this cohort study. The patients were divided into two groups: the delayed APS diagnosis group (APS-d) (n=40) and the timely APS diagnosis group (APS-t) (n=32).72.2% patients showed relieved ischemia symptoms (APS-d vs APS-t, p=0.035), 27.8% patients showed recurrence of thrombosis, and 23.6%patients needed further surgery (APS-d vs APS-t, p=0.042). 37.5% APS patients were administered intravenous immunoglobulin (IVIG) (APS-d vs APS-t, p<0.01) and 34.8% were administered hormonotherapy (APS-d vs APS-t, p<0.01). The rate of amputation was 19.4% (APS-d vs APS-t, p=0.049) and the mortality rate was 16.6% (APS-d vs APS-t, p=0.033).Delayed diagnosis of APS in ALI patients was associated with a high risk of amputation and mortality. ALI patients who were diagnosed with APS early and underwent timely initiation of hormonotherapy, IVIG and anticoagulation, showed improved amputation and mortality.