自噬
转化研究
疾病
医学
神经科学
生物信息学
生物
细胞凋亡
病理
遗传学
作者
Tianyi Wang,Haochen Jiang,Ruwen Zheng,Chuchu Zhang,MA Xiu-mei,Yi Liu
标识
DOI:10.1177/13872877251336442
摘要
Background Alzheimer's disease (AD) is characterized by amyloid-β plaques and tau aggregates, with autophagy dysfunction playing a key pathogenic role. While autophagy modulation shows therapeutic promise, comprehensive bibliometric analyses are lacking. Objective This study aims to map the research landscape of autophagy in AD through bibliometric analysis, identifying key trends, contributors, and emerging focus areas. Methods We analyzed 4018 publications (2003–2023) from Web of Science using VOSviewer and CiteSpace. Publication trends, influential authors, countries, institutions, and research hotspots were examined through co-occurrence, burst detection, and clustering analyses. Results Annual publications have steadily increased, peaking in 2022. The US led in output and citations, with major contributions from the University of California and New York University. Ralph A. Nixon emerged as the most influential author. Early research (2003–2013) primarily focused on protein degradation mechanisms, whereas recent studies (2014–2023) emphasize mitochondrial dysfunction, apoptosis, and related pathways. Key evolving topics include endoplasmic reticulum stress and chaperone-mediated autophagy, with significant implications for therapeutic innovation. Conclusions Autophagy plays a critical role in AD pathogenesis and represents a promising therapeutic target. Despite mechanistic advances, clinical translation remains challenging. Future research should prioritize multi-omics integration, drug delivery optimization, and managing risks associated with excessive autophagy activation. These findings provide valuable insights for developing novel AD therapies targeting autophagy.
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