Evidence map›Paper›PMID 41770449›Full record

ArticleJournal of endocrinological investigation2026

Biglycan knockdown improves Graves' orbitopathy (GO)-like features via inhibiting NF-kB and ERK signaling.

Changci Chenzhao, Min Zhu, Feng Zhang, Bingyu Xie, Jiamin Cao, Wei Xiong, Yao Tan

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Article in Journal of endocrinological investigation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Changci ChenzhaoDepartment of Ophthalmology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Min ZhuDepartment of Ophthalmology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Feng ZhangDepartment of Ophthalmology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Bingyu XieDepartment of Ophthalmology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Jiamin CaoDepartment of Ophthalmology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Wei XiongDepartment of Ophthalmology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China. weixiong420@csu.edu.cn.ORCID http://orcid.org/0000-0002-3017-9895
Yao TanDepartment of Ophthalmology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China. tanyao2000@csu.edu.cn.

Funding

National Natural Science Foundation of China 82371104Natural Science Foundation of Hunan Province 2023JJ30851
6 · The paper itself

Abstract

purposeGraves' orbitopathy (GO) is an autoimmune disease characterized by orbital inflammation, fibroblast activation, and adipogenesis, with limited effective therapies. This study aimed to investigate the role of biglycan (BGN) in GO pathogenesis and its underlying mechanisms.

methodsBioinformatic analyses were performed to identify differentially expressed genes in GO tissues. BGN protein levels were validated in orbital adipose tissues from GO patients. Functional effects of BGN were examined by overexpression or knockdown in human GO orbital fibroblasts (GO-OFs) in vitro. In vivo, a thyroid-associated ophthalmopathy (TAO) mouse model was used to evaluate the effects of Bgn knockdown on orbital fibrosis and adipogenesis.

resultsBGN expression was significantly upregulated in GO orbital tissues. In vitro, BGN overexpression promoted, while BGN knockdown attenuated, fibrosis and adipogenesis in GO-OFs. Mechanistically, BGN activated nuclear factor kappa B (NF-κB) and extracellular signal-regulated kinase (ERK) signaling pathways. In vivo, Bgn knockdown reduced GO-like pathological features, including fibrosis and adipose expansion, and decreased NF‑κB and ERK signaling activation.

conclusionBGN contributes to fibrosis and adipogenesis in GO via NF‑κB and ERK signaling activation. These findings elucidate a pivotal role for BGN in GO pathogenesis and highlight its potential as a therapeutic target for GO treatment.

Indexed as

BiglycanGraves OphthalmopathyMAP Kinase Signaling SystemNF-kappa BAdipogenesisAdipose TissueAnimalsCells, CulturedDisease Models, AnimalFemaleFibroblastsFibrosisGene Knockdown TechniquesHumansMiceSignal TransductionBGN protein, humanBiglycanNF-kappa BAdipogenesisBiglycan (BGN)ERKNF-κBOrbital fibroblastThyroid-associated ophthalmopathy (TAO)

Identifiers

PMID41770449

What Socratic holds

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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 Socratic graph.