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ABHD1通过调节糖尿病视网膜病变中的KRT1和KRT2促进中间丝介导的内皮细胞趋化性。

ABHD1 Facilitates Intermediate Filament-Mediated Endothelial Cell Chemotaxis by Regulating KRT1 and KRT2 in Diabetic Retinopathy.

作者信息

Liu Xinyi, Fang Junwei, Niu Tian, Xing Xindan, Shi Xin, Xiao Yu, Qu Yuan, Jiang Yan, Lv Kangjia, Dou Tianyu, Zhu Qian, Wan Hancong, Liu Xiaoxin, Wang Hanying, Liu Kun

机构信息

Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China.

National Clinical Research Center for Eye Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China.

出版信息

J Diabetes Res. 2024 Nov 20;2024:5513165. doi: 10.1155/jdr/5513165. eCollection 2024.

DOI:10.1155/jdr/5513165
PMID:39619568
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11606687/
Abstract

Diabetic retinopathy (DR) is one of the most common complications of diabetes and induces severe visual impairment worldwide. Endothelial cell dysfunction plays an important role in the pathogenesis of DR. Here, we keep a watchful eye on /-hydrolase domain-containing 1 (ABHD1), a potential regulator in lipid metabolism and neovascularization. Results revealed that ABHD1 expression increased both in retina tissues of DR patients and in high-glucose-treated human retina endothelial cells. Inhibition of ABHD1 remitted endothelial cell proliferation and migration. And GSEA uncovered that ABHD1 knockdown remits endothelial cell chemotaxis and intermediate filament (IF) might be mediated in the progress by regulating keratin 1 (KRT1) and keratin 2 (KRT2). Therefore, we assume that ABHD1 is concerned with endothelial cell proliferation and migration in DR, consequently leading to pathological neovascularization. The findings may provide a potential therapeutic target for DR.

摘要

糖尿病视网膜病变(DR)是糖尿病最常见的并发症之一,在全球范围内导致严重的视力损害。内皮细胞功能障碍在DR的发病机制中起重要作用。在此,我们关注含α/β-水解酶结构域1(ABHD1),它是脂质代谢和新生血管形成的潜在调节因子。结果显示,ABHD1在DR患者的视网膜组织以及高糖处理的人视网膜内皮细胞中表达均增加。抑制ABHD1可减轻内皮细胞的增殖和迁移。基因集富集分析(GSEA)发现,敲低ABHD1可减轻内皮细胞趋化性,并且中间丝(IF)可能通过调节角蛋白1(KRT1)和角蛋白2(KRT2)在这一过程中发挥介导作用。因此,我们推测ABHD1与DR中内皮细胞的增殖和迁移有关,进而导致病理性新生血管形成。这些发现可能为DR提供一个潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e10/11606687/cd2fb7adab6b/JDR2024-5513165.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e10/11606687/9d7d52050d00/JDR2024-5513165.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e10/11606687/b3dad2862841/JDR2024-5513165.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e10/11606687/25587ec42833/JDR2024-5513165.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e10/11606687/6356b2bdfa41/JDR2024-5513165.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e10/11606687/f8560bb8e736/JDR2024-5513165.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e10/11606687/cd2fb7adab6b/JDR2024-5513165.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e10/11606687/9d7d52050d00/JDR2024-5513165.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e10/11606687/b3dad2862841/JDR2024-5513165.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e10/11606687/25587ec42833/JDR2024-5513165.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e10/11606687/6356b2bdfa41/JDR2024-5513165.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e10/11606687/f8560bb8e736/JDR2024-5513165.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e10/11606687/cd2fb7adab6b/JDR2024-5513165.006.jpg

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本文引用的文献

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Mechanistic Pathogenesis of Endothelial Dysfunction in Diabetic Nephropathy and Retinopathy.
糖尿病肾病和视网膜病变中内皮功能障碍的发病机制。
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Keratin 1 as a cell-surface receptor in cancer.角蛋白 1 作为癌症中的细胞表面受体。
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Association between ABHD1 and DOK6 polymorphisms and susceptibility to Hirschsprung disease in Southern Chinese children.ABHD1 和 DOK6 多态性与中国南方儿童先天性巨结肠病易感性的关联。
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