目的:慢性疼痛在心理生理、治疗性的,经济负担,不仅限于成人,还包括儿科年龄。尽管影响很大,其分子机制尚未完全阐明。关注表观遗传学对疼痛复杂性状的影响,我们评估了慢性疼痛与TRPA1甲基化模式之间的关联,TRPA1是与疼痛敏感性相关的关键基因.
方法:我们从三个不同的数据库检索文章进行了系统综述。重复数据删除后,431个项目进行了手动筛选,然后选择61篇文章并再次筛选。其中,仅保留6个用于荟萃分析,并使用特定R包进行分析.
结果:六篇文章分为两组(第1组:健康受试者和慢性疼痛患者之间的平均甲基化水平比较;第2组:平均甲基化水平与疼痛感觉之间的相关性)。从第1组的分析中获得非显著性平均差异,值为3.97(95%C.I.-7.79;15.73)。对第2组的分析显示,由于异质性(I2=97%,因此研究之间的变异性很高(相关性=0.35,95%C.I.-0.12;0.82),p<0.01)。
结论:尽管在分析的不同研究中观察到了高度的变异性,我们的结果表明,高甲基化和疼痛敏感性增加可能是有联系的,可能是由于TRPA1表达的变化。
Chronic pain represents a major global health issue in terms of psycho-physiological, therapeutic, and economic burden, not limited to adults but also to the pediatric age. Despite its great impact, its molecular mechanisms have still not been completely unraveled. Focusing on the impact of epigenetics in the pain complex trait, we assessed the association between chronic pain and the methylation pattern of TRPA1, a key gene related to pain sensitivity.
We conducted a systematic
review retrieving articles from three different databases. After deduplication, 431 items were subjected to manual screening, and then 61 articles were selected and screened again. Of these, only six were maintained for meta-analysis and analyzed using specific R packages.
Six articles were divided into two groups (group 1: comparison of mean methylation levels between healthy subjects and patients with chronic pain; group 2: correlation between mean methylation levels and pain sensation). A non-significant mean difference was obtained from the analysis of group 1 with a value of 3.97 (95% C.I. -7.79; 15.73). Analysis of group 2 showed a high level of variability between studies (correlation = 0.35, 95% C.I. -0.12; 0.82) due to their heterogeneity (I2 = 97%, p < 0.01).
Despite the high variability observed in the different studies analyzed, our results suggest that hypermethylation and increased pain sensitivity could be connected, possibly due to the variation of TRPA1 expression.