高血压相关听力损失的趋势与机制见解：2005-2025年二十年视角

文献信息

中文摘要

引言： 高血压和听力损失（HL）在快速老龄化的社会中日益普遍，构成重大公共卫生挑战；现有证据提示两者之间可能存在关联。尽管高血压与HL的关联已受到广泛关注，但对于二者共存的潜在分子相互作用机制以及该领域的整体研究趋势，仍缺乏深入探索和系统总结。
方法： 从Web of Science核心合集、Scopus和PubMed检索2005年至2025年的出版物；纳入2,351条记录，并使用Bibliometrix、CiteSpace和VOSviewer进行分析。同时，使用GeneCards、GEO和STRING识别并整合相关分子靶点和通路。
结果： 总体发文量呈持续上升趋势，美国和中国的贡献最为突出。关键词和聚类分析突出了衰老和性别相关主题（如“aged”、“male”），并提示研究从描述性临床观察转向病因学和治疗学探究。作者和机构层面分析表明，Frank Robert Lin、哈佛大学和约翰斯·霍普金斯大学在该领域高度活跃且具有影响力。基因交集分析识别出高血压与HL之间共享的903个基因；IL1A、TGFB1、EGFR、MMP9、TP53、ICAM1和BCL2成为突出的网络节点。对GeneCards来源基因和GEO来源差异表达基因的富集分析一致涉及AGE-RAGE、PI3K-Akt和cGMP-PKG信号通路、流体剪切应力与动脉粥样硬化，以及涉及氧化应激反应和血液循环调节的生物学过程。
结论： 这些发现支持将听力风险分层和早期筛查纳入高血压管理，并提供了一个可操作的多靶点策略的机制框架，可能有助于更早识别和干预，并减少后续治疗负担。

英文摘要

INTRODUCTION: Hypertension and hearing loss (HL) are increasingly prevalent in rapidly aging societies and pose major public health challenges; existing evidence suggests a potential association between the two. Although the association between hypertension and HL has received extensive attention, there is still a lack of in-depth exploration and systematic summary regarding the potential molecular interaction mechanisms underlying their coexistence, as well as the overall research trends in this field.
METHODS: Publications from 2005 to 2025 were retrieved from the Web of Science Core Collection, Scopus, and PubMed; 2,351 records were included and analyzed using Bibliometrix, CiteSpace, and VOSviewer. In parallel, GeneCards, GEO, and STRING were used to identify and integrate relevant molecular targets and pathways.
RESULTS: Overall publication output showed a sustained upward trend, with the United States and China contributing most prominently. Keyword and clustering analyses highlighted aging- and sex-related themes (such as "aged," "male") and suggested a shift from descriptive clinical observations toward etiological and therapeutic investigations. Author- and institution-level analyses indicated that Frank Robert Lin, Harvard University, and Johns Hopkins University were highly active and influential in this field. Gene intersection analysis identified 903 genes shared between hypertension and HL; IL1A, TGFB1, EGFR, MMP9, TP53, ICAM1, and BCL2 emerged as prominent network nodes. Enrichment analyses of GeneCards-derived genes and GEO-derived differentially expressed genes consistently implicated the AGE-RAGE, PI3K-Akt, and cGMP-PKG signaling pathways, fluid shear stress and atherosclerosis, as well as biological processes involving the response to oxidative stress and the regulation of blood circulation.
CONCLUSION: These findings support incorporating hearing risk stratification and early screening into hypertension management and provide a mechanistic framework for actionable multi-target strategies, potentially enabling earlier identification and intervention and reducing subsequent treatment burden.