Trial reportPloS one2011
Genome-wide gene expression analysis suggests an important role of hypoxia in the pathogenesis of endemic osteochondropathy Kashin-Beck disease.
Trial report in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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.
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.
Who cites it
11 citing papers in PubMed, 35 citations in OpenAlex.
- Identification of HIF-1α/VEGFA signaling pathway and transcription factors in Kashin-Beck disease by integrated bioinformatics analysis.Experimental and therapeutic medicine · 2021Article
- Genome-Wide Association Analysis Identified ANXA1 Associated with Shoulder Impingement Syndrome in UK Biobank Samples.G3 (Bethesda, Md.) · 2020Article
- Comparison of microRNA expression profiles of Kashin-Beck disease, osteoarthritis and rheumatoid arthritis.Scientific reports · 2017Article
- Investigation of MMP-1 genetic polymorphisms and protein expression and their effects on the risk of Kashin-Beck disease in the northwest Chinese Han population.Journal of orthopaedic surgery and research · 2016Article
- The effects of T-2 toxin on the prevalence and development of Kashin-Beck disease in China: a meta-analysis and systematic review.Toxicology research · 2016Review
- Gene expression signature in endemic osteoarthritis by microarray analysis.International journal of molecular sciences · 2015Article
- COL9A1 gene polymorphism is associated with Kashin-Beck disease in a northwest Chinese Han population.PloS one · 2015Article
- Serum levels of M-CSF, RANKL and OPG in rats fed with Kashin-Beck disease-affected diet.Journal of orthopaedic surgery and research · 2014Article
- Whole-exome sequencing for the identification of susceptibility genes of Kashin-Beck disease.PloS one · 2014Article
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kashin-Beck Disease (KBD) is an endemic osteochondropathy, the pathogenesis of which remains unclear now. In this study, we compared gene expression profiles of articular cartilage derived respectively from KBD patients and normal controls. Total RNA were isolated, amplified, labeled and hybridized to Agilent human 1A 22 k whole genome microarray chip. qRT-PCR was conducted to validate our microarray data. We detected 57 up-regulated genes (ratios ≥2.0) and 24 down-regulated genes (ratios ≤0.5) in KBD cartilage. To further identify the key genes involved in the pathogenesis of KBD, Bayesian analysis of variance for microarrays (BAM) software was applied and identified 12 potential key genes with an average ratio 6.64, involved in apoptosis, metabolism, cytokine & growth factor and cytoskeleton & cell movement. Gene Set Enrichment Analysis (GSEA) software was used to identify differently expressed gene ontology categories and pathways. GSEA found that a set of apoptosis, hypoxia and mitochondrial function related gene ontology categories and pathways were significantly up-regulated in KBD compared to normal controls. Based on the results of this study, we suggest that chronic hypoxia-induced mitochondrial damage and apoptosis might play an important role in the pathogenesis of KBD. Our efforts may help to understand the pathogenesis of KBD as well as other osteoarthrosis with similar articular cartilage lesions.
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