| Description |
Osteoporosis is a disease that impacts the elderly. Reduced estrogen has been related to changes in DNA methylation and consequent alterations in gene expression in a number of studies, leading to a new direction for research into the pathophysiology of osteoporosis. As a consequence, the OVX mouse model was constructed in our study, and it was found that the mouse models were indeed osteoporosis by studying the phenotype and methylation level in the mouse's bone, and at the same time, the methylation level of the OVX mice were significantly changed compared to that of SHAM mice. As a consequence, we performed genome-level analysis on the mouse model using transcriptome and WGBS. We discovered that the changes in gene expression level caused by osteoporosis mainly focus on the decrease of bone and muscle development and the activation of the immune system by combining the data of two omics. These differentially expressed genes and pathways are consistent with the differentially expressed methylation locations and regions, according to intersection analysis of methylation and transcriptome data. We found that the differentially expressed methylation sites of these genes are mainly concentrated in promoters, Exons, and other important functional regions by selecting important differentially expressed genes. This is also the primary cause of gene differential expression variations, indicating that estrogen deficiency might further regulate gene expression by altering methylation modification, leading to the development of osteoporosis. At the same time, the clinical value of methylation modification research is demonstrated in this research. The findings are expected to add to current understanding of the molecular mechanisms underlying osteoporosis incidence and development, as well as provide new ideas for early detection and treatment of osteoporosis. |
