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Timp2修饰的明胶羟基苯丙酸水凝胶可逆转小鼠巩膜恢复增强并抑制近视发展。

Timp2-modified gelatinhydroxyphenylpropionic acid hydrogels reverse enhanced scleral recovery and suppress myopia development in mice.

作者信息

Liu Kaiqi, Li Ting, Gu Lingwen, Jiang Zhenyu, Jiang Jing, Yang Xi, Zhou Yang, Feng Xiao, Gong Qianqian, Zhao Lihua, Chen Yiming, Yang Chao, Jiang Tao

机构信息

Department of Ophthalmology, The Affiliated Hospital of Qingdao University, Qingdao, 266003, China.

Department of Ophthalmology, The Qingdao University Affiliated Women and Children's Hospital, Qingdao, 266011, China.

出版信息

Mater Today Bio. 2025 Jun 7;33:101942. doi: 10.1016/j.mtbio.2025.101942. eCollection 2025 Aug.

DOI:10.1016/j.mtbio.2025.101942
PMID:40677403
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12268941/
Abstract

A novel therapeutic strategy for form deprivation myopia (FDM) involving Timp2-modified scleral stem cells (SSC) embedded in gelatin-hydroxyphenylpropionic acid (Gtn-HPA) hydrogel was investigated. Transcriptome and single-cell RNA sequencing analyses identified Timp2 as a crucial factor in FDM progression due to its reduced expression in FDM sclera. The developed SSC-Gtn-HPA hydrogel composite demonstrated excellent biocompatibility, rapid gelation, and degradation properties. studies showed that SSC-GH promoted human scleral fibroblast (HSF) proliferation, inhibited apoptosis, and prevented differentiation. experiments in mice showed that SSC-GH effectively regulated ocular parameters, facilitated scleral recovery, and improved FDM conditions. These results highlight the potential of SSC-GH as a promising therapeutic approach for myopia treatment by enhancing scleral recovery.

摘要

研究了一种针对形觉剥夺性近视(FDM)的新型治疗策略,该策略涉及嵌入明胶-羟苯丙酸(Gtn-HPA)水凝胶中的Timp2修饰的巩膜干细胞(SSC)。转录组和单细胞RNA测序分析确定Timp2是FDM进展中的关键因素,因为它在FDM巩膜中的表达降低。所开发的SSC-Gtn-HPA水凝胶复合材料表现出优异的生物相容性、快速凝胶化和降解性能。研究表明,SSC-GH促进人巩膜成纤维细胞(HSF)增殖,抑制细胞凋亡,并防止分化。在小鼠身上进行的实验表明,SSC-GH有效地调节眼部参数,促进巩膜恢复,并改善FDM状况。这些结果突出了SSC-GH通过增强巩膜恢复作为一种有前景的近视治疗方法的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e16/12268941/7c86a841ac32/mmcfigs5.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e16/12268941/c862896b9adf/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e16/12268941/eae148f9aca4/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e16/12268941/faa150874d7a/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e16/12268941/8284422f4425/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e16/12268941/381540b1d920/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e16/12268941/028e47fafbdd/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e16/12268941/93f9c3fdcb61/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e16/12268941/f6098329f3e0/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e16/12268941/988c4c9f720e/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e16/12268941/b9ea90e6d12e/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e16/12268941/0fa48d395b34/mmcfigs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e16/12268941/1d8efbb00a07/mmcfigs2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e16/12268941/7c86a841ac32/mmcfigs5.jpg

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J Mater Chem B. 2024 Mar 6;12(10):2559-2570. doi: 10.1039/d3tb02548a.
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FOXM1 Participates in Scleral Remodeling in Myopia by Upregulating APOA1 Expression Through METTL3/YTHDF2.
FOXM1 通过上调 APOA1 表达通过 METTL3/YTHDF2 参与近视巩膜重塑。
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