Global research trends and hotspots of PI3K/Akt signaling pathway in the field of osteoarthritis: A bibliometric study

Medicine (Baltimore). 2023 Apr 14;102(15):e33489. doi: 10.1097/MD.0000000000033489.

Abstract

The phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway has gradually become a new target for the treatment of osteoarthritis (OA). Numerous studies of PI3K/Akt signaling in OA have been published in the past few years. By analyzing these research characteristics and qualities, we aimed to reveal the current research focus and emerging trends in PI3K/Akt signaling in OA. We searched the Web of Science database for relevant articles concerning the PI3K/Akt signaling pathway in OA published from inception to October 31, 2022. The following data were extracted: author name, article title, keywords, topic, publication country/region, institution, publication journal, journal impact factor, number of times cited, and H-index. VOSviewer and Excel 2019 were used to conduct the bibliometric study and visualize the analysis. A total of 374 publications were included in this study. In all selected articles, "orthopedics" was the dominant topic (252 of 374, 67.38%). The most productive year was 2021. Frontiers in Pharmacology published the most articles. The People's Republic of China has published the most articles worldwide. The top 5 keywords were "OA," "expression," "apoptosis," "chondrocytes," and "inflammation." The keywords "autophagy," "mitochondrial dysfunction," "inflammatory response," "cartilage degeneration," and "network pharmacology" have increased in recent years. Our study showed a growing trend in published articles related to the PI3K/Akt signaling pathway in OA. Inflammatory response, cartilage degeneration, and apoptosis remain central topics in the field. Research on autophagy, mitochondrial dysfunction, and network pharmacology is on the rise, and the focus on PI3K/Akt will continue to increase.

MeSH terms

  • Bibliometrics
  • Humans
  • Osteoarthritis*
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt*
  • Signal Transduction

Substances

  • Proto-Oncogene Proteins c-akt
  • Phosphatidylinositol 3-Kinases