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Analysis highlighted extracellular matrix and structural organization signatures, enriched PI3K-AKT and AMPK signaling pathways, and a protein–protein interaction network suggesting molecular disease mechanisms and candidate therapy 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[https://doi.org/10.1155/genr/5540232](https://doi.org/10.1155/genr/5540232)  \nResearch Article  \nMethylation Landscapes of Cartilage in Hip Osteoarthritis  \nRuiyang Jiang , 1 Maochun Wang ,2,3 Guihua Tan,3 Jie Lv,3 Xiaoyu Jin,4 Yuan Liu,3 Rui Wu,3 and Dongquan Shi 1,3,4  \n1 Division of Sports Medicine and Adult Reconstructive Surgery, Department of Orthopedic Surgery,  \nNanjing Drum Tower Hospital Clinical College of Xuzhou Medical University, 321 Zhongshan Road,  \nNanjing 210008, Jiangsu, China  \n2 Department of Plastic Surgery, Te Afliated Friendship Plastic Surgery Hospital of Nanjing Medical University, Nanjing, Jiangsu, China  \n3 Division of Sports Medicine and Adult Reconstructive Surgery, Department of Orthopedic Surgery,  \nNanjing Drum Tower Hospital, Te Afliated Hospital of Nanjing University Medical School, Nanjing, China  \n4 Division of Sports Medicine and Adult Reconstructive Surgery, Department of Orthopedic Surgery,  \nNanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing, China  \nCorrespondence should be addressed to Dongquan Shi; [shidongquan@nju.edu.cn](shidongquan@nju.edu.cn)  \nReceived 5 January 2025; Revised 27 August 2025; Accepted 12 December 2025  \nAcademic Editor: Yingkun Xu  \nCopyright © 2026 Ruiyang Jiang et al. Genetics Research published by John Wiley & Sons Ltd. Tis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.  \nObjective: To elucidate diferent methylation landscapes between cartilage of femoral neck fracture and preserved and damaged cartilages in hip osteoarthritis (OA) .  \nMethods: Genome-wide DNA methylation data were acquired from two data sets in GEO database (GSE63106 and GSE63695), which were based on Illumina HumanMethylation450 BeadChip arrays. A total of 63 hip samples were selected for further analysis, including 19 cartilages obtained from patients with femoral neck fracture, 14 preserved cartilages, and 30 damaged cartilages obtained from patients with OA. We identifed the diferential methylated positions (DMPs) and genes between diferent cartilage groups.  \nResults: Tere were 116,750 DMPs and 51,200 DMPs identifed in preserved and damaged cartilages compared to cartilage in femoral neck fracture, respectively, while there were no signals found between preserved and damaged cartilages. Gene ontology analysis showed that most of diferential methylated genes were enriched in extracellular matrix and structure organization, collagen-containing extracellular matrix, and KEGG enrichment highlighted PI3K-AKT and AMPK signaling pathways, which were known to be crucial for the progression of OA. Further construction of protein–protein interaction networks with differential methylated genes elucidated molecular basis of the disease. Tree hypermethylated genes (NOTCH1, GREM1, and DYSF) and three hypomethylated genes (HDAC4, S100A10, and RUNX1) were selected to detect the relative expression in diferent cartilages, and their expression was correlated with the methylation status within the genes.  \nConclusion: We demonstrated the diferential methylated genes across the whole genome not only on preserved cartilage but also on damaged cartilage during OA. Te molecular network highlighted the potential therapy targets which may be involved in the initiation or progression of the disease.  \nKeywords: AMPK; cartilage; genome-wide DNA methylation; hip osteoarthritis; PI3K-AKT  \n1. Introduction  \nOsteoarthritis (OA) is a common degenerative joint disease, which is characterized by destruction of articular cartilage  \nand accompanied by changes in other joint tissues [1–3] . It is widely known that a lot of risk factors are responsible for OA, including aging, gender, obesity, genetics, and epigenetics [4, 5] . Genetic approaches using genome-","cbCaib8fjWovrZlw","https://ap.wps.com/l/cbCaib8fjWovrZlw","pdf",3948857,13,"English","# Objective\n# Methods\n# Results\n# Conclusion\n# Introduction","[{\"question\":\"What was the study objective regarding cartilage methylation in hip osteoarthritis?\",\"answer\":\"The study aimed to elucidate different methylation landscapes between femoral neck fracture cartilage and preserved or damaged cartilage in hip osteoarthritis.\"},{\"question\":\"How were the genome-wide DNA methylation datasets obtained and analyzed?\",\"answer\":\"Genome-wide DNA methylation data were acquired from GEO datasets GSE63106 and GSE63695 using Illumina HumanMethylation450 BeadChip arrays, followed by identification of differential methylated positions (DMPs) and genes across cartilage groups.\"},{\"question\":\"What key biological pathways and gene categories were enriched in the results?\",\"answer\":\"Gene ontology and KEGG enrichment emphasized extracellular matrix and structure organization, and highlighted PI3K-AKT and AMPK signaling pathways, with protein–protein interaction networks supporting molecular basis of OA progression.\"}]","Methylation Landscapes of Cartilage in Hip Osteoarthritis | PDF",1790687374,33]