在多中心骨关节炎研究 (MOST) 中评估表观遗传年龄加速与骨关节炎的关联
Michelle S Yau1, Paul C Okoro2, Ida K Haugen3
1Marcus Institute for Aging Research, Hebrew SeniorLife, Boston, MA, USA; Division of Gerontology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Osteoarthritis and cartilage
|January 19, 2024
概括
表观遗传年龄加速,生物衰老的衡量标准,在45-69岁成年人的研究中没有显示与骨关节炎风险增加的联系. 这一发现表明,时间上的年龄仍然是骨关节炎发展的主要因素.
科学领域:
- 老年学和表观遗传学
- 骨关节炎的发病原因
- 生物标志物发现发现
背景情况:
- 年龄的增长是骨关节炎 (OA) 的重要危险因素.
- 源自DNA甲基化模式的表观遗传衰老加速可能为OA相关的衰老机制提供了洞察力.
- 了解这些机制可以为OA的预防和治疗策略提供信息.
研究的目的:
- 调查表观遗传衰老加速与患膝盖,手和多关节性关节炎的风险之间的关联.
- 为了确定表观遗传年龄加速是否能预测骨关节炎的风险,而不依赖于时间年龄.
主要方法:
- 分析了多中心骨关节炎研究中671名参与者 (年龄在45-69岁) 的数据.
- 使用Illumina Infinium MethylationEPIC 850K阵列进行评估的DNA甲基化.
- 使用Hannum,Horvath,PhenoAge和GrimAge时钟计算表观遗传年龄;将表观遗传年龄回归到时间年龄来得出残余值 (年龄加速).
- 逻辑回归用于评估表观遗传年龄加速残留物与膝盖,手和多关节的X光OA之间的关联,调整为共变量.
主要成果:
- 放射性骨关节炎的发病率:23%的手,25%的膝盖,8%的多关节.
- 平均时间年龄为58.4岁;平均预测的表观遗传年龄从50.5 (PhenoAge) 到68.6 (Hannum) 之间.
- 在经过对时间年龄和其他因素进行调整后,在表观遗传年龄加速 (使用Horvath,Hannum,PhenoAge或GrimAge时钟) 与手,膝盖或多关节OA增加的几率之间没有发现显著的关联.
结论:
- 用已建立的DNA甲基化钟来测量表观遗传年龄加速,与患膝盖,手或多关节性关节炎的风险增加无关.
- 这些发现表明,在这一群体中,与年龄相关的关节炎风险的主要因素是时间的年龄,而不是表观遗传的年龄加速.
- 进一步的研究可能会探索与OA病变发生有关的其他表观遗传修饰或生物途径.
更多相关视频
07:22Glycemic Impact on Knee Osteoarthritis Symptoms on Physical, Radiographic, and Inflammatory Markers among Individuals Aged 50 and Over with Diabetes
Published on: March 7, 2025
230
07:32Standardized Histomorphometric Evaluation of Osteoarthritis in a Surgical Mouse Model
Published on: May 6, 2020
12.1K
相关概念视频
Genome-wide Association Studies-GWAS
13.4K
Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
GWAS does not require the identification of the target gene involved in...
GWAS does not require the identification of the target gene involved in...
13.4K
Bone Disorders
3.5K
Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
3.5K
Epigenetic Regulation
3.0K
Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
X-chromosome...
3.0K
