儿童肥胖与性早熟共病的文献计量及共享靶点分析

Bibliometric and shared target analysis of the comorbidity of childhood obesity and precocious puberty

摘要

目的 基于文献计量学与生物信息学方法, 系统分析儿童肥胖与性早熟相关研究的演进趋势, 并探讨二者潜在共享分子机制。方法 检索Web of Science Core Collection 中2005 年1 月至2026 年3 月有关儿童肥胖与性早熟的文献, 采用VOSviewer 和CiteSpace 对发文趋势、国家、机构、作者合作及关键词演化进行可视化分析；同时整合GeneCards、OMIM 和DrugBank 数据库筛选共享靶点, 构建蛋白质-蛋白质相互作用（PPI）网络, 并开展基因本体（GO）、京都基因与基因组百科全书（KEGG）及疾病本体（DO）富集分析。结果 共纳入214篇文献, 发文量总体呈上升趋势, 美国和中国为主要研究贡献国家。关键词分析显示, 该领域研究重心已由早期流行病学描述逐步转向代谢异常、神经内分泌调控及环境相关机制。共筛得1 392个共享基因, PPI 网络提示TP53、AKT1、CTNNB1、ESR1、EP300、STAT3、EGFR和MYC可能为核心节点。富集分析显示, 共享基因主要涉及转录调控、激素反应和信号转导等生物过程, 并显著富集于PI3K-Akt、MAPK、FoxO、cAMP 及AGE-RAGE 等信号通路。结论 儿童肥胖与性早熟相关研究正由表型关联分析转向机制整合研究, AKT1、TP53、ESR1等核心基因及PI3K-Akt、AGE-RAGE 等通路可能在二者共病中发挥重要作用, 为后续机制研究及早期干预提供了线索。

Abstract

Objective To systematically analyze the evolving trends in research on childhood obesity and precocious puberty using bibliometric and bioinformatic methods, and to explore their potential shared molecular mechanisms. Methods The articles on childhood obesity and precocious puberty published between January 2005 and March 2026 were retrieved from the Web of Science Core Collection. VOSviewer and CiteSpace were used to visualize publication trends, collaborations among countries, institutions and authors, as well as keyword evolution. Concurrently, shared targets were identified by integrating the GeneCards, OMIM, and DrugBank databases. A protein-protein interaction network was constructed, followed by GO, KEGG, and DO enrichment analyses. Results A total of 214 articles were included. The annual publication output showed an overall upward trend, with the United States and China being the major contributing countries. Keyword analysis revealed that the research focus in this field had gradually shifted from epidemiological descriptions in the early stage to mechanisms involving metabolic abnormalities, neuroendocrine regulation, and environmental factors. A total of 1 392 shared genes were identified. The protein-protein interaction network suggested that TP53, AKT1, CTNNB1, ESR1, EP300, STAT3, EGFR, and MYC might serve as core nodes. Enrichment analyses indicated that the shared genes primarily involved the biological processes such as transcriptional regulation, hormone response and signal transduction, and were significantly enriched in signaling pathways including PI3K-Akt, MAPK, FoxO, cAMP, and AGE-RAGE. Conclusion Researches on childhood obesity and precocious puberty are shifting from phenotypic association analysis to integrated mechanistic investigation. Core genes such as AKT1, TP53, and ESR1, along with pathways including PI3K-Akt and AGE-RAGE, may play important roles in the comorbidity of these two conditions, providing clues for future mechanistic studies and early intervention.

关键词

肥胖 / 性早熟 / 共病 / 文献计量学 / 共享靶点 / 儿童

Key words

Obesity / Precocious puberty / Comorbidity / Bibliometrics / Shared targets / Child

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基金资助

厦门市儿童青少年肥胖中医药干预试点工作项目(厦卫中医〔2024〕264号)