DOI 10.2174/0118715273398806251024072412
Research Prospects for mTOR in Neuroinflammation: A Bibliometric Analysis.
Аннотация
INTRODUCTION
Neuroinflammation is a key pathological process in neurological disorders, from acute injuries to chronic diseases such as Alzheimer's Disease (AD), Parkinson's Disease (PD), and stroke. The mTOR pathway regulates neuroinflammation by influencing microglial activation, autophagy, and synaptic plasticity. To address the scarcity of systematic analyses in this growing field, our study employs bibliometric analysis to map the landscape, identify key themes and collaborations, and highlight therapeutic targets for future neurological research.
METHODS
A Web of Science search retrieved articles published up to 2024. Bibliometric analysis and visualization were conducted using VOSviewer, CiteSpace, Charticulator, and Microsoft Excel.
RESULTS
A total of 509 articles were examined, showing a fluctuating increase in publications and citations. China had the highest output, and the Journal of Neuroinflammation was the most active journal. Mehan Sidharth emerged as a leading researcher. The most cited study was "HIF1α- dependent glycolytic pathway orchestrates a metabolic checkpoint for the differentiation of TH17 and Treg cells". Findings revealed strong links between neuroinflammation and AD, PD, and stroke, and highlighted mTOR inhibitors as promising therapeutic agents.
DISCUSSION: Our analysis identified highly-cited works, current trends, emerging frontiers, and the significance of mTOR inhibitors. However, the comprehensiveness of our bibliometric approach may have been limited by the field's vast scope and by analytical disparities between CiteSpace and VOSviewer, potentially resulting in omissions.
CONCLUSION
This study provides an overview of scientific progress on mTOR signaling and neuroinflammation, emphasizing its key role in disease mechanisms and suggesting directions for therapeutic innovation.
Предметные рубрики MeSH
Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
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