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Reversal of persistent wound-induced retinal pigmented epithelial-to-mesenchymal transition by the TGFb pathway inhibitor, A-83-01.

ChEBI2015-07-06 更新2026-07-12 收录

视网膜病变机制

TGFb通路抑制剂研究

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-67898 数据链接链接失效反馈

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Reversal of persistent wound-induced retinal pigmented epithelial-to-mesenchymal transition by the TGFb pathway inhibitor, A-83-01.

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创建时间：

2015-07-06

视网膜病变机制

基因治疗模型开发

Purpose: We constructed and characterized knockout and conditional knockout mice for KCNJ13, encoding the inwardly rectifying K+ channel of the Kir superfamily Kir7.1, mutations in which cause both Sn

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Paired-class homeodomain transcription factors (HD TFs) play essential roles in vertebrate development, and their mutations are linked to human diseases. One unique feature of paired-class HD is coope

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Profiles of N6-methyladenosine modifications of circular RNAs in oxygen-induced retinopathy. Profiles of N6-methyladenosine modifications of circular RNAs in oxygen-induced retinopathy

表观转录组学

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To identify the N6-methyladenosine (m6A) modified circular RNAs (circRNAs) involved in a mouse model of oxygen-induced retinopathy (OIR), microarray analysis was performed with the retinal samples fro

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Rising from the dead: A novel mechanism involving pyroptosis and pathologic neovascularization in retinopathy of prematurity

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To elucidate the changes in retinal angiogenesis, we performed single-cell RNA sequencing on OIR model isolated retinal cells.We found the specific expression of AIP1 gene in endothelial cells, which

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Transcriptomic comparison of 3D retinal organoids derived from retinitis pigmentosa patient harboring PDE6B mutation and non-phenotype control

视网膜病变机制

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Retinitis pigmentosa (RP) is a hereditary retinal degenerative disease. Although an increasing number of disease genes have been identified, the exact cellular mechanisms of RP remain largely unclear

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Reversal of persistent wound-induced retinal pigmented epithelial-to-mesenchymal transition by the TGFb pathway inhibitor, A-83-01.

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