非遗传性肥胖类型网络和新药点:一种在的方法
Styliani A Geronikolou1,2, Athanasia Pavlopoulou3,4, Merve Uça Apaydin3,4
1Clinical, Translational Research and Experimental Surgery Centre, Biomedical Research Foundation of the Academy of Athens, 4, Soranou Ephessiou Str., 11527 Athens, Greece.
International journal of molecular sciences
|July 27, 2024
概括
这项研究绘制了非遗传性肥胖症中的基因网络图,揭示了压力和炎症途径. 它确定了潜在的治疗点和天然化合物用于治疗肥胖症.
科学领域:
- 遗传学和系统生物学 系统生物学
- 代谢障碍 代谢障碍 代谢障碍
- 时间生物学 时间生物学
背景情况:
- 肥胖是一种慢性,可预防的疾病,由于伴随性疾病,其社会成本很高.
- 了解非遗传性肥胖的致病性对于确定治疗点至关重要.
- 生物钟基因在能量平衡和代谢调节中发挥作用.
研究的目的:
- 重建非遗传性肥胖的互动组,以阐明病原性.
- 为了确定肥胖的潜在治疗点.
- 发现针对肥胖和生理时钟相关蛋白质的天然化合物.
主要方法:
- 从PubMed,GeneCards和OMIM中提取了与肥胖和生物钟相关的基因.
- 使用STRING v11.0研究的基因/蛋白质相互作用具有高可信度评分 (>0.7).
- 应用虚拟选来识别针对相关蛋白质的自然化合物.
主要成果:
- 开发了两个相互作用体:压力诱导 (85个基因) 和炎症诱导 (93个基因) 肥胖体.
- 确定了两个相互作用体之间的15个共同基因,包括关键的代谢和激素调节者 (例如,LEP,INS,MC4R).
- 菲利格里丁E被确定为潜在的FOX1-DBD相互作用阻断剂.
结论:
- 分子网络提供了对能量平衡和肥胖病原体的综合调节的见解.
- 这些发现可能会将慢性药理与天然产品联系起来,用于新型肥胖治疗.
- 已识别的相互作用和化合物为治疗干预提供了潜在的途径.
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