Evidence map›Paper›PMID 41547890›Full record

ArticleScientific reports2026

GOLGB1 deficiency accelerates intervertebral disc degeneration by activating the MAPK pathway.

Jingyuan Tian, Zhiquan Wang, Ruxing Liu, Xiaoting Qiu, Dongqin He, Nan Shan, Qichao Li, Guanghui He, Bin Zhao, Jie Yuan and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 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

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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

11 authors.

Jingyuan Tian *Department of Orthopedics, Second Hospital of Shanxi Medical University, Taiyuan, 030001, China.
Zhiquan Wang *Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Shanxi Medical University, Taiyuan, 030001, China.
Ruxing LiuDepartment of Shanxi key Laboratory of Bone and Soft Tissue Injury Repair, Second Hospital of Shanxi Medical University, Taiyuan, 030001, China.
Xiaoting QiuDepartment of Shanxi key Laboratory of Bone and Soft Tissue Injury Repair, Second Hospital of Shanxi Medical University, Taiyuan, 030001, China.
Dongqin HeDepartment of Shanxi key Laboratory of Bone and Soft Tissue Injury Repair, Second Hospital of Shanxi Medical University, Taiyuan, 030001, China.
Nan ShanDepartment of Shanxi key Laboratory of Bone and Soft Tissue Injury Repair, Second Hospital of Shanxi Medical University, Taiyuan, 030001, China.
Qichao LiDepartment of Shanxi key Laboratory of Bone and Soft Tissue Injury Repair, Second Hospital of Shanxi Medical University, Taiyuan, 030001, China.
Guanghui HeDepartment of Shanxi key Laboratory of Bone and Soft Tissue Injury Repair, Second Hospital of Shanxi Medical University, Taiyuan, 030001, China.
Bin ZhaoDepartment of Shanxi key Laboratory of Bone and Soft Tissue Injury Repair, Second Hospital of Shanxi Medical University, Taiyuan, 030001, China. zzbb3737@126.com.
Jie YuanDepartment of Shanxi key Laboratory of Bone and Soft Tissue Injury Repair, Second Hospital of Shanxi Medical University, Taiyuan, 030001, China. messiyj@sina.com.
Yongfeng WangDepartment of Shanxi key Laboratory of Bone and Soft Tissue Injury Repair, Second Hospital of Shanxi Medical University, Taiyuan, 030001, China. wyfwf8@163.com.

Funding

Natural Science Foundation for Young Scientists of Shanxi Province 20210302124670Shanxi Province Higher Education "Billion Project" Science and Technology Guidance Project BYJL013Shanxi Province Higher Education "Billion Project" Science and Technology Guidance Project BYJL030Shanxi Provincial Science and Technology Cooperation and Exchange Special Project 202104041101023The Natural Science Foundation of Shanxi Province, China 202203021211040
6 · The paper itself

Abstract

Intervertebral disc degeneration (IDD) is a multifactorially regulated age-related condition. Golgin B1 (GOLGB1) is a large Golgi-related transmembrane protein encoded by golgb1 gene. Since its discovery, GOLGB1 has been proved to be related to many diseases. However, its role in IDD is still unclear. The aim of this research was to examine whether GOLGB1 deficiency accelerates disc degeneration and to study its mechanism. We selected C57BL/6 male mice aged 8 weeks to isolate, culture and identify nucleus pulposus (NP) cells, and used a variety of experimental techniques, including plasmid transfection, western blotting (WB), real-time fluorescence quantitative PCR (RT-qPCR), EdU staining, Tunnel staining, CCK8 and flow cytometry (FCM) to detect the effects of GOLGB1 on the degeneration, proliferation and apoptosis of NP cells in vitro. Then, 8-week-old C57BL/6 male mice were selected for caudal vertebra acupuncture to establish IDD model, and the role and mechanism of GOLGB1 in the development of IDD were studied by HE staining, Safranin O-Fast Green staining, Alcian Blue staining and immunohistochemistry (IHC) staining. Our results demonstrated lower expression of GOLGB1 in human tissues with NP degeneration. Additionally, GOLGB1 expression was reduced in NP tissue from aging adult mice and IDD model mice. We further verified that GOLGB1 knockdown worsened NP cell degeneration, disturbed the composition of the extracellular matrix (ECM), and upset the harmony between anabolism and catabolism. Moreover, GOLGB1 knockdown inhibited the proliferation of NP cells and increased the apoptosis of NP cells. Mechanistically, GOLGB1 knockdown elevated p-ERK and p-P38 levels and activated the MAPK pathway. A MAPK signaling pathway inhibitor (SCH772984) strongly reversed this phenomenon and rescued the degeneration of NP cells. These findings suggest that GOLGB1 may be a potential new target for IDD. GOLGB1 is a protective factor against disc degeneration, and knockdown of GOLGB1 accelerates IDD by activating the MAPK pathway.

Indexed as

Intervertebral Disc DegenerationMAP Kinase Signaling SystemMembrane ProteinsAnimalsApoptosisCell ProliferationDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLNucleus PulposusMembrane ProteinsApoptosisExtracellular matrixGOLGB1Intervertebral disc degenerationMAPK pathwayProliferation

Identifiers

PMID41547890
PMCPMC12887002

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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 OpenQuestion graph.