دورية أكاديمية
Omentin reduces venous neointimal hyperplasia in arteriovenous fistula through hypoxia-inducible factor-1 alpha inhibition.
| العنوان: | Omentin reduces venous neointimal hyperplasia in arteriovenous fistula through hypoxia-inducible factor-1 alpha inhibition. |
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| المؤلفون: | Zhui L; Department of Vascular Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China. Electronic address: lizhui0511@126.com., Yuling C; Department of Vascular Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China., Hansheng W; Department of Vascular Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China., Xiangjie L; Department of Vascular Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China. |
| المصدر: | Microvascular research [Microvasc Res] 2024 Jul; Vol. 154, pp. 104688. Date of Electronic Publication: 2024 Apr 18. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Academic Press Country of Publication: United States NLM ID: 0165035 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1095-9319 (Electronic) Linking ISSN: 00262862 NLM ISO Abbreviation: Microvasc Res Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: New York, Academic Press. |
| مواضيع طبية MeSH: | Hyperplasia* , Neointima* , Hypoxia-Inducible Factor 1, alpha Subunit*/metabolism , Hypoxia-Inducible Factor 1, alpha Subunit*/genetics , Cytokines*/metabolism , GPI-Linked Proteins*/metabolism , GPI-Linked Proteins*/pharmacology , GPI-Linked Proteins*/genetics , Disease Models, Animal* , Cell Proliferation*/drug effects , Signal Transduction* , Myocytes, Smooth Muscle*/pathology , Myocytes, Smooth Muscle*/metabolism , Myocytes, Smooth Muscle*/drug effects , Lectins*/pharmacology , Lectins*/metabolism , Cell Movement*/drug effects , Muscle, Smooth, Vascular*/pathology , Muscle, Smooth, Vascular*/metabolism , Muscle, Smooth, Vascular*/drug effects , AMP-Activated Protein Kinases*/metabolism , Arteriovenous Shunt, Surgical*/adverse effects, Animals ; Rabbits ; Humans ; Cells, Cultured ; Male ; Kidney Failure, Chronic/pathology ; TOR Serine-Threonine Kinases/metabolism ; Graft Occlusion, Vascular/pathology ; Graft Occlusion, Vascular/prevention & control ; Graft Occlusion, Vascular/metabolism ; Graft Occlusion, Vascular/physiopathology ; Jugular Veins/pathology ; Jugular Veins/metabolism ; Jugular Veins/transplantation |
| مستخلص: | Arteriovenous fistula (AVF) failure often involves venous neointimal hyperplasia (VNH) driven by elevated hypoxia-inducible factor-1 alpha (HIF-1α) in the venous wall. Omentin, known for its anti-inflammatory and anti-hyperplasia properties, has an uncertain role in early AVF failure. This study investigates omentin's impact on VNH using a chronic renal failure (CRF) rabbit model. The CRF rabbit model of AVF received omentin-expressing adenoviral vector or control β-gal vector to assess omentin's effects on VNH. Human vascular smooth muscle cells (HVSMCs), stimulated with tumor necrosis factor-α (TNF-α), were exposed to recombinant human omentin (Rh-OMT) to study its influence on cell proliferation and migration. The AMP-activated protein kinase (AMPK) inhibitor compound C and the mammalian target of rapamycin (mTOR) activator MHY1485 were employed to explore omentin's mechanisms in VNH reduction through HIF-1α inhibition. Omentin treatment reduced VNH in CRF rabbits, concomitant with HIF-1α down-regulation and the suppression of downstream factors, including vascular endothelial growth factor and matrix metalloproteinases. Rh-OMT inhibited TNF-α-induced HVSMC proliferation and migration by modulating both cell cycle and cell adhesion proteins. Additionally, omentin reduced HIF-1α expression through the AMPK/mTOR pathway activation. Notably, the blockade of AMPK/mTOR signaling reversed omentin-mediated inhibition of VNH, cell proliferation, and migration, both in vivo and in vitro. In conclusion, omentin mitigates VNH post-AVF creation by restraining HIF-1α via AMPK/mTOR signaling. Strategies boosting circulating omentin levels may offer promise in averting AVF failure. Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. (Copyright © 2024 Elsevier Inc. All rights reserved.) |
| فهرسة مساهمة: | Keywords: Arteriovenous fistula; Chronic renal failure; Hypoxia-inducible factor-1α; Omentin; Venous neointimal hyperplasia |
| المشرفين على المادة: | 0 (Hypoxia-Inducible Factor 1, alpha Subunit) 0 (Cytokines) 0 (GPI-Linked Proteins) 0 (Lectins) 0 (ITLN1 protein, human) EC 2.7.11.31 (AMP-Activated Protein Kinases) 0 (HIF1A protein, human) EC 2.7.11.1 (TOR Serine-Threonine Kinases) EC 2.7.1.1 (MTOR protein, human) |
| تواريخ الأحداث: | Date Created: 20240419 Date Completed: 20240615 Latest Revision: 20240705 |
| رمز التحديث: | 20240706 |
| DOI: | 10.1016/j.mvr.2024.104688 |
| PMID: | 38640999 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1095-9319 |
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| DOI: | 10.1016/j.mvr.2024.104688 |