Evidence map›Paper›PMID 41257962›Full record

ArticleMolecular cytogenetics2025

SLC8A1 as a novel susceptibility gene in facilitating tendinopathy: insights into its mechanisms from Mendelian randomization and experimental validation.

Junjie Tang, Weijie Wu, Ziqi Zhou, Peng Shen, Jianye Liu, Xinyuan Wu, Minhao Chen, Hua Xu

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Article in Molecular cytogenetics, 2025. 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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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

8 authors.

Junjie Tang *Department of Orthopaedics, Medical School of Nantong University, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Weijie Wu *Department of Orthopaedics, Affiliated Nantong Hospital of Shanghai University, The Sixth People's Hospital of Nantong, Nantong, 226001, China.
Ziqi Zhou *Department of Orthopaedics, Medical School of Nantong University, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Peng ShenDepartment of Orthopaedics, Nantong Tongzhou People's Hospital, Nantong, 226001, China.
Jianye LiuDepartment of Orthopaedics, Medical School of Nantong University, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Xinyuan WuDepartment of Orthopaedics, Medical School of Nantong University, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Minhao ChenDepartment of Orthopaedics, Medical School of Nantong University, Affiliated Hospital of Nantong University, Nantong, 226001, China. chenminhao_nt@126.com.
Hua XuDepartment of Orthopaedics, Medical School of Nantong University, Affiliated Hospital of Nantong University, Nantong, 226001, China. xuhuantu@yeah.net.

Funding

China Postdoctoral Science Foundation 2022M711718Jiangsu Provincial Research Hospital YJXYY202204Natural Science Foundation of Nantong JC2023098Scientific Research Project of Nantong Commission of Health MS2023022
6 · The paper itself

Abstract

backgroundPatients with tendinopathy (TD) have expressed dissatisfaction with the efficacy of the first-line treatment, indomethacin. This research aims to identify key biomarkers in TD and investigate their underlying mechanisms.

methodsTendon samples were harvested from 5 Sprague-Dawley (SD) rats exhibiting TD and 5 healthy normal controls (NCs), destined for transcriptome sequencing. After thorough preprocessing of the RNA sequencing data, a differential expression analysis was performed to identify genes that significantly differentiated the TD group from the NCs. To identify candidate genes, an intersection analysis was performed between the differentially expressed genes (DEGs) and the key module genes obtained through weighted gene co-expression network analysis. The candidate genes underwent Mendelian randomization (MR) analysis and least absolute shrinkage and selection operator analysis to identify key genes. We conducted experimental validation and sensitivity analyses, such as pleiotropy, heterogeneity, and leave-one-out evaluations, to ensure the robustness of our findings.

resultsThe findings present new evidence indicating that SLC8A1 facilitates the progression of TD. MR analysis established a causal link between SLC8A1 and TD progression (p < 0.05). The study indicated that SLC8A1 might inhibit TD progression by negatively regulating gamma-glutamylisoleucine levels. In SD rats, TD led to a disordered arrangement of collagen structures, increased infiltration of inflammatory cells, increased cell density, and thicker inflammatory hyperplasia in tendon. These results confirm the effective creation of a TD model. Analysis showed significant upregulation of SLC8A1 expression in the TD group (p < 0.05).

conclusionThis research highlights SLC8A1 as a potential biomarker in TD development, providing novel perspectives for clinical diagnosis and treatment strategies.

Indexed as

Achilles tendon injuryGamma − glutamylisoleucineMendelian randomizationSLC8A1Tendinopathy

Identifiers

PMID41257962
PMCPMC12628930

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