Transcription factor SP1 drives TGF-β1-induced transformation of human tenon's capsule fibroblasts by transcription activation-mediated SNAI2 upregulation.

Yiying Chen, Yirong Chen, Chunmei Li, Zongkai Bai, Han Yang, Qianqian Wang, Yaqin Zhang

Abstract read

In one paragraph

Article in International ophthalmology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing papers in PubMed

–field-weighted citation impact

1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

[Silybin inhibits fibrosis after glaucoma filtration surgery in rabbits by promoting fibroblast autophagy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
Article

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Yiying Chen *Department of Ophthalmology, Pu'er People's Hospital, Pu'er, 665000, Yunnan, China.

Yirong Chen *Department of Nutrition, Pu'er People's Hospital, Pu'er, 665000, Yunnan, China.

Chunmei LiDepartment of Laboratory, Lancang County Disease Prevention and Control Center, Pu'er, 665000, Yunnan, China.

Zongkai BaiDepartment of Reproductive Genetics, Pu'er People's Hospital, Pu'er, 665000, Yunnan, China.

Han YangDepartment of Reproductive Genetics, Pu'er People's Hospital, Pu'er, 665000, Yunnan, China.

Qianqian WangDepartment of Respiratory and Critical Care Medicine, Pu'er People's Hospital, Pu'er, 665000, Yunnan, China.

Yaqin ZhangDepartment of Reproductive Genetics, Pu'er People's Hospital, Pu'er, 665000, Yunnan, China. zhangyaqinya@163.com.

Funding

Kunming University of Science and Technology - Puer People's Hospital Medical Joint Project KUST-PE2022016YOpen Project of Yunnan Clinical Medical Center 2022LCZXKF-SZ14Special Project of Key Laboratory for Prevention and Control of Ophthalmic Diseases in Yunnan Province 2017DG008(2023)-2

6 · The paper itself

Abstract

backgroundGlaucoma is an irreversible blinding disease worldwide with complex pathogenesis. Previous studies have indicated that Specificity protein 1 (SP1) plays a critical role in diverse diseases, including glaucoma. This study is designed to explore the role and underlying mechanism of SP1 in the development of glaucoma.

methodsSP1 and Snail Family Transcriptional Repressor 2 (SNAI2) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). SP1, SNAI2, Fibronectin, α-SMA, E-cadherin, LC3BI, LC3BII, and p62 protein levels were assessed using western blot assay. Binding between SP1 and SNAI2 promoter was predicted by JASPAR and validated using Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays. Cell viability, migration, and invasion were measured using Cell Counting Kit-8 (CCK-8), transwell, and wound healing assays.

resultsSP1 and SNAI2 were highly expressed in glaucoma patients and transforming growth factor beta-1 (TGF-β1)-treated human Tenon's capsule fibroblast cells (HTFs). At the molecular level, SP1 was a transcription factor of SNAI2 and increased the transcriptional activity of SNAI2 by binding to its promoter region. SP1 knockdown could relieve TGF-β1-induced HTF viability, migration, invasion, extracellular matrix (ECM) deposition, and autophagy.

conclusionSP1-activated SNAI2 transcription promotes TGF-β1-triggered HTF viability, migration, invasion, ECM deposition, and autophagy, which provides a promising therapeutic target for glaucoma treatment.

Indexed as

FibroblastsGene Expression RegulationGlaucomaSnail Family Transcription FactorsSp1 Transcription FactorTenon CapsuleTranscriptional ActivationTransforming Growth Factor beta1Blotting, WesternCell MovementCells, CulturedHumansReal-Time Polymerase Chain ReactionUp-RegulationSNAI2 protein, humanSnail Family Transcription FactorsSP1 protein, humanSp1 Transcription FactorTransforming Growth Factor beta1AutophagyGlaucomaSNAI2SP1TGF-β1

Identifiers

PMID40504458

DOI10.1007/s10792-025-03581-8

What OpenQuestion holds

Textmetadata

Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.