Evidence map›Paper›PMID 41082466›Full record

ArticleIET systems biology

PGK1: A Common Biomarker and Therapeutic Target Linking Sarcopenia and Osteoporosis Through Fibroblast-Mediated Pathways.

Kun Zhang, Hailong Li, Xinhong Chen, Ping Tang, Meng Wang, Chunting Yang, Rong Su, Xiaqin Gao, Fan Zhang, Juan Han

Abstract read
In one paragraph

Article in IET systems biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

10 authors.

Kun ZhangDepartment of Trauma Orthopedics, Gansu Provincial Traditional Chinese Medicine Hospital, Lanzhou, China.
Hailong LiDepartment of General Practice, Luohu Clinical College, School of Medicine, Shantou University, Shenzhen, China.ORCID 0000-0002-5972-907X
Xinhong ChenDepartment of General Practice, Luohu Clinical College, School of Medicine, Shantou University, Shenzhen, China.
Ping TangDepartment of General Practice, Luohu Clinical College, School of Medicine, Shantou University, Shenzhen, China.
Meng WangDepartment of Internal Medicine, First School of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, China.
Chunting YangDepartment of Internal Medicine, First School of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, China.
Rong SuDepartment of Internal Medicine, First School of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, China.
Xiaqin GaoDepartment of Internal Medicine, First School of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, China.
Fan ZhangDepartment of Geriatrics, Affiliated Hospital of Gansu University of Traditional Chinese Medicine, Lanzhou, China.
Juan HanDepartment of Trauma Orthopedics, Gansu Provincial Traditional Chinese Medicine Hospital, Lanzhou, China.

Funding

Entrepreneurship Project of Science and Technology Bureau of Chengguan District of Lanzhou city #Chengke [2023] No. 38, 2023-2-5Shenzhen Key Medical Discipline Construction Fund No.SZXK062
6 · The paper itself

Abstract

Sarcopenia and osteoporosis share pathophysiological links, but their co-occurrence mechanisms remain unclear. This study aimed to identify molecular mediators of their co-development using bioinformatics. Datasets for sarcopenia (GSE56815) and osteoporosis (GSE9103) were retrieved from GEO. Differentially expressed genes (DEGs) were analysed via edgeR and limma. Gene ontology (GO), Kyoto encyclopaedia of genes and genomes (KEGG) and weighted gene co-expression network analysis (WGCNA) identified shared pathways and hub genes. Protein-protein interaction (PPI) networks were constructed using STRING and Cytoscape. We validated hub genes in independent datasets (GSE13850, GSE8479) and assessed via ROC curves. Immune infiltration, single-cell analysis and drug prediction were performed. We identified 134 common DEGs (30 upregulated, 104 downregulated). WGCNA and PPI analysis revealed 14 hub genes (APOE, CDK2, PGK1, HRAS, RUNX2 etc.), all with ROC-AUC > 0.6. PGK1 was consistently downregulated in both diseases and linked to 21 miRNAs and six transcription factors (HSF1, TP53, JUN etc.). Single-cell analysis localised PGK1 predominantly in skeletal muscle fibroblasts. DrugBank identified lamivudine as a potential PGK1-targeting therapeutic. PGK1 emerged as a central downregulated gene in sarcopenia and osteoporosis, enriched in fibroblasts and modulated by lamivudine. These findings highlight PGK1 as a shared diagnostic and therapeutic target, offering insights into musculoskeletal crosstalk.

Indexed as

FibroblastsOsteoporosisPhosphoglycerate KinaseSarcopeniaBiomarkersComputational BiologyGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksHumansProtein Interaction MapsSignal TransductionBiomarkersPGK1 protein, humanPhosphoglycerate Kinasebig databioinformaticsdata analysismolecular dynamics methodnetwork analysissignal transduction

Identifiers

PMID41082466
PMCPMC12517354

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Registered trials

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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.