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非遗传性肥胖类型网络与新药靶标:一种计算方法。

Non-Hereditary Obesity Type Networks and New Drug Targets: An In Silico Approach.

机构信息

Clinical, Translational Research and Experimental Surgery Centre, Biomedical Research Foundation of the Academy of Athens, 4, Soranou Ephessiou Str., 11527 Athens, Greece.

University Research Institute of Maternal and Child Health and Precision Medicine, National and Kapodistrian University of Athens Medical School, Levadias 8, 11527 Athens, Greece.

出版信息

Int J Mol Sci. 2024 Jul 12;25(14):7684. doi: 10.3390/ijms25147684.

Abstract

Obesity, a chronic, preventable disease, has significant comorbidities that are associated with a great human and financial cost for society. The aim of the present work is to reconstruct the interactomes of non-hereditary obesity to highlight recent advances of its pathogenesis, and discover potential therapeutic targets. Obesity and biological-clock-related genes and/or gene products were extracted from the biomedical literature databases PubMed, GeneCards and OMIM. Their interactions were investigated using STRING v11.0 (a database of known and predicted physical and indirect associations among genes/proteins), and a high confidence interaction score of >0.7 was set. We also applied virtual screening to discover natural compounds targeting obesity- and circadian-clock-associated proteins. Two updated and comprehensive interactomes, the (a) stress- and (b) inflammation-induced obesidomes involving 85 and 93 gene/gene products of known and/or predicted interactions with an average node degree of 9.41 and 10.8, respectively, were produced. Moreover, 15 of these were common between the two non-hereditary entities, namely, ADIPOQ, ADRB2/3, CCK, CRH, CXCL8, FOS, GCG, GNRH1, IGF1, INS, LEP, MC4R, NPY and POMC, while phelligridin E, a natural product, may function as a potent FOX1-DBD interaction blocker. Molecular networks may contribute to the understanding of the integrated regulation of energy balance/obesity pathogenesis and may associate chronopharmacology schemes with natural products.

摘要

肥胖是一种慢性、可预防的疾病,具有显著的合并症,给社会带来了巨大的人力和经济成本。本工作旨在重建非遗传性肥胖的相互作用组,以突出其发病机制的最新进展,并发现潜在的治疗靶点。从生物医学文献数据库 PubMed、GeneCards 和 OMIM 中提取肥胖和生物钟相关基因和/或基因产物。使用 STRING v11.0(已知和预测的基因/蛋白质之间的物理和间接关联的数据库)研究它们的相互作用,并设置了>0.7 的高置信度相互作用评分。我们还应用虚拟筛选来发现针对肥胖和生物钟相关蛋白的天然化合物。两个更新和全面的相互作用组,(a)应激和(b)炎症诱导的肥胖组,涉及 85 和 93 个基因/基因产物,它们具有已知和/或预测的相互作用,平均节点度分别为 9.41 和 10.8。此外,这两个非遗传性实体之间有 15 个是共同的,即 ADIPOQ、ADRB2/3、CCK、CRH、CXCL8、FOS、GCG、GNRH1、IGF1、INS、LEP、MC4R、NPY 和 POMC,而天然产物 phelligridin E 可能作为一种有效的 FOX1-DBD 相互作用阻断剂发挥作用。分子网络可能有助于理解能量平衡/肥胖发病机制的综合调控,并将chronopharmacology方案与天然产物联系起来。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9a7/11277295/84e07abd650a/ijms-25-07684-g005.jpg

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