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脂肪酸去饱和酶1基因敲低促进糖尿病角膜上皮的伤口愈合和功能恢复。

Fatty Acid Desaturase 1 Knockdown Promotes Wound Healing and Functional Recovery of the Corneal Epithelium in Diabetes.

作者信息

Zhao Yangqi, Dong Yi, Zheng Qingqing, Zhao Yue, Ni Yingjie, Qiu Peijin, Chen Chuannan, Xu Mengyue, Hong Chaoyang, Shen Ting

机构信息

Department of Ophthalmology, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China.

Eye Center, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.

出版信息

Invest Ophthalmol Vis Sci. 2025 Jun 2;66(6):6. doi: 10.1167/iovs.66.6.6.

DOI:10.1167/iovs.66.6.6
PMID:40459498
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12136103/
Abstract

PURPOSE

Fatty acid desaturase 1 (FADS1) is significantly and specifically upregulated following diabetic corneal injury. However, its role in diabetic keratopathy remains unclear. This study aimed to investigate the impact of FADS1 on wound healing and functional recovery of the diabetic corneal epithelium and explore its potential mechanisms.

METHODS

Using high-glucose-induced corneal epithelial cells and a streptozotocin-induced type 1 diabetic mouse model, FADS1 expression was suppressed via FADS1 small interfering RNA (siRNA). Cell migration was assessed using scratch and transwell assays. Wound healing and functional recovery of the corneal epithelium were evaluated using sodium fluorescein staining, anterior segment optical coherence tomography, hematoxylin and eosin staining, and immunofluorescence staining.

RESULTS

FADS1 knockdown promoted wound healing and functional recovery of the diabetic corneal epithelium both in vivo and in vitro. Suppression of FADS1 enhanced high-glucose-induced corneal epithelial cell migration, which was dependent on elevated levels of the upstream metabolite γ-linolenic acid. This effect was mediated through the activation of the mitogen-activated protein kinase signaling pathway and the accumulation of autophagosomes.

CONCLUSIONS

After diabetic corneal epithelial injury, FADS1 expression is specifically upregulated. Knockdown of FADS1 promotes wound healing and functional recovery, suggesting a novel therapeutic strategy for diabetic keratopathy.

摘要

目的

脂肪酸去饱和酶1（FADS1）在糖尿病性角膜损伤后显著且特异性地上调。然而，其在糖尿病性角膜病变中的作用仍不清楚。本研究旨在探讨FADS1对糖尿病性角膜上皮伤口愈合和功能恢复的影响，并探讨其潜在机制。

方法

使用高糖诱导的角膜上皮细胞和链脲佐菌素诱导的1型糖尿病小鼠模型，通过FADS1小干扰RNA（siRNA）抑制FADS1表达。使用划痕试验和Transwell试验评估细胞迁移。使用荧光素钠染色、眼前节光学相干断层扫描、苏木精-伊红染色和免疫荧光染色评估角膜上皮的伤口愈合和功能恢复。

结果

FADS1基因敲低促进了糖尿病性角膜上皮在体内和体外的伤口愈合和功能恢复。抑制FADS1可增强高糖诱导的角膜上皮细胞迁移，这依赖于上游代谢产物γ-亚麻酸水平的升高。这种作用是通过丝裂原活化蛋白激酶信号通路的激活和自噬体的积累介导的。

结论

糖尿病性角膜上皮损伤后，FADS1表达特异性上调。FADS1基因敲低促进伤口愈合和功能恢复，提示糖尿病性角膜病变的一种新的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/bea04592a0af/iovs-66-6-6-f009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/1501c5fcb5c0/iovs-66-6-6-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/b56be11fa866/iovs-66-6-6-f002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/10752f6d1871/iovs-66-6-6-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/83dbc4528732/iovs-66-6-6-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/d6a31bce7c2c/iovs-66-6-6-f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/54f060e3a840/iovs-66-6-6-f008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/bea04592a0af/iovs-66-6-6-f009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/1501c5fcb5c0/iovs-66-6-6-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/b56be11fa866/iovs-66-6-6-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/ebed6143bcb4/iovs-66-6-6-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/da3505766a7f/iovs-66-6-6-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/10752f6d1871/iovs-66-6-6-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/83dbc4528732/iovs-66-6-6-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/d6a31bce7c2c/iovs-66-6-6-f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/54f060e3a840/iovs-66-6-6-f008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a079/12136103/bea04592a0af/iovs-66-6-6-f009.jpg

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RTP4 Enhances Corneal HSV-1 Infection in Mice With Type 2 Diabetes Mellitus.
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