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敲低HCK可通过调节AMPK信号通路促进人视网膜内皮细胞(HREC)的细胞活力和视网膜内血液屏障完整性。

Knockdown of HCK promotes HREC cell viability and inner blood-retinal barrier integrity by regulating the AMPK signaling pathway.

作者信息

Chen Lu, Lin Chengmin

机构信息

Ophthalmology Teaching and Research Office, Zhejiang Industry & Trade Vocational College, Wenzhou, Zhejiang, 325000, China.

Department of Ophthalmology, Wenzhou Hospital of Integrated Traditional Chinese and Western Medicine, No.75 Jinxiu Road, Wenzhou, Zhejiang, 325000, China.

出版信息

Open Life Sci. 2024 Sep 3;19(1):20220924. doi: 10.1515/biol-2022-0924. eCollection 2024.

DOI:10.1515/biol-2022-0924
PMID:39247797
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11377936/
Abstract

Diabetic retinopathy (DR), a major complication of diabetes causing blindness, is characterized by retinal damage due to capillary degeneration and vascular leakage. Current treatments are not fully effective, highlighting the need for searching new therapeutic targets. Hematopoietic cell kinase (HCK), a protein involved in various diseases, has been identified as a potential biomarker in DR, but its role in disease progression requires further investigation. Here we investigated the role of HCK in DR and its potential mechanism. We found the expression of HCK increased under the stimulation of high glucose (HG) in human retinal capillary endothelial cells (HRECs). Knockdown of HCK can improve HREC cell viability and the integrity of the internal blood-retinal barrier. HCK depletion suppressed the AMPK pathway in HG-induced HRECs. In summary, HCK may be a potential target for the treatment of DR, which provides a theoretical basis for the development of new treatment strategies.

摘要

糖尿病视网膜病变(DR)是导致失明的糖尿病主要并发症,其特征是由于毛细血管变性和血管渗漏引起视网膜损伤。目前的治疗方法并不完全有效,这凸显了寻找新治疗靶点的必要性。造血细胞激酶(HCK)是一种与多种疾病相关的蛋白质,已被确定为DR中的潜在生物标志物,但其在疾病进展中的作用需要进一步研究。在此,我们研究了HCK在DR中的作用及其潜在机制。我们发现,在高糖(HG)刺激下,人视网膜毛细血管内皮细胞(HREC)中HCK的表达增加。敲低HCK可提高HREC细胞活力和血视网膜内屏障的完整性。HCK缺失抑制了HG诱导的HREC中的AMPK通路。总之,HCK可能是治疗DR的潜在靶点,为开发新的治疗策略提供了理论依据。

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本文引用的文献

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Advanced Glycation End Products Upregulate CD40 in Human Retinal Endothelial and Müller Cells: Relevance to Diabetic Retinopathy.晚期糖基化终末产物上调人视网膜内皮细胞和 Müller 细胞中的 CD40:与糖尿病视网膜病变的关系。
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糖尿病视网膜病变致盲——综述。
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Platycodin D inhibits diabetic retinopathy via suppressing TLR4/MyD88/NF-κB signaling pathway and activating Nrf2/HO-1 signaling pathway.桔梗皂苷 D 通过抑制 TLR4/MyD88/NF-κB 信号通路和激活 Nrf2/HO-1 信号通路来抑制糖尿病视网膜病变。
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Diabetic Retinopathy: Clinical Features, Risk Factors, and Treatment Options.糖尿病视网膜病变:临床特征、危险因素和治疗选择。
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