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多聚体肿瘤坏死因子相关凋亡诱导配体抑制大鼠动静脉吻合和球囊损伤诱导的新生内膜增生。

Suppression of neointimal hyperplasia induced by arteriovenous anastomosis and balloon injury in rats by multimeric tumor necrosis factor-related apoptosis-inducing ligand.

机构信息

Department of Biochemistry, Chosun University School of Medicine, Gwangju 61452, Republic of Korea.

Surgery Department, Chang Surgical Clinic, Gwangju 62274, Republic of Korea.

出版信息

Mol Cells. 2024 Jun;47(6):100075. doi: 10.1016/j.mocell.2024.100075. Epub 2024 May 31.

Abstract

Excessive blood vessel wall thickening, known as intimal hyperplasia, can result from injury or inflammation and increase the risk of vascular diseases. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) plays key roles in tumor surveillance, autoimmune diseases, and apoptosis; however, its role in vascular stenosis remains controversial. Treatment with recombinant isoleucine zipper hexamerization domain soluble TRAIL (ILz(6):TRAIL) significantly inhibited the progression of neointimal hyperplasia (NH) induced by anastomosis of the carotid artery and jugular vein dose dependently, and adenovirus expressing secretable ILz(6):TRAIL also inhibited NH induced by balloon injury in the femoral artery of rats. This study demonstrated the preventive and partial regressive effects of ILz(6):TRAIL on anastomosis of the carotid artery and jugular vein- or balloon-induced NH.

摘要

血管壁过度增厚,即内膜增生,可能由损伤或炎症引起,并增加血管疾病的风险。肿瘤坏死因子相关凋亡诱导配体(TRAIL)在肿瘤监测、自身免疫性疾病和细胞凋亡中发挥关键作用;然而,其在血管狭窄中的作用仍存在争议。用重组异亮氨酸拉链六聚体结构域可溶性 TRAIL(ILz(6):TRAIL)治疗可显著抑制颈动脉和颈静脉吻合诱导的新生内膜增生(NH)的进展,呈剂量依赖性,表达可分泌 ILz(6):TRAIL 的腺病毒也可抑制大鼠股动脉球囊损伤诱导的 NH。本研究证明了 ILz(6):TRAIL 对颈动脉和颈静脉吻合或球囊诱导的 NH 的预防和部分消退作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64ce/11227017/0c891ab78ac9/gr1.jpg

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