Title:Bibliometric Analysis and Systemic Review of Cantharidin Research
Worldwide
Volume: 25
Issue: 12
Author(s): Tianmu He, Cancan Duan, Wenzhong Feng, Jingwen Ao, Dingyang Lu, Xiaofei Li*Jianyong Zhang*
Affiliation:
- School of Basic Medicine, Zunyi medical University, Zunyi 550025, China
- School of Basic Medicine, Guizhou
Medical University, Guiyang 563000, Guizhou, China
- School of Pharmacy and Key Laboratory of Basic Pharmacology
Ministry Education and Joint International Research Laboratory of Ethnomedicine, Ministry of Education, Zunyi
Medical University, Zunyi 563000, Guizhou, China
Keywords:
Bibliometric, cantharidin, pharmacology, protein phosphatase 2A, toxic mechanism, hepatocellular carcinoma, surgical resection.
Abstract:
Background: Cantharidin (CTD), a natural toxic compound from blister beetle
Mylabris, has been used for cancer treatment for millenary. CTD and its analogs have become
mainstream adjuvant drugs with radiotherapy and chemotherapy in clinical applications. However,
the detailed pharmacology mechanism of CTD was not fully elucidated.
Methods: Publications of CTD were collected from the Web of Science Core Collection database
from 1991 to 2023 using CiteSpace, VOSviewer, and Scimago Graphica software.
Results: A total of 1,611 publications of CTD were mainly published in China and the United
States. The University of Newcastle has published the most researches. Mcclusey, Adam, Sakoff,
Jennette, and Zhang, Yalin had the most CTD publications with higher H. Notably, CTD
researches were mainly published in Bioorganic & Medicinal Chemistry Letters and the Journal
of Biological Chemistry. Cluster profile results revealed that protein phosphatase 2A (PP2A),
human gallbladder carcinoma, Aidi injection, and cell apoptosis were the hotspots. Concentration
on the pharmacology function of PP2A subunit regulation, hepatotoxicity, nephrotoxicity,
and cardiotoxicity mechanism should be strengthened in the future.
Conclusion: Bibliometric analysis combined with a systemic review of CTD research first revealed
that PP2A and CTD analogs were the knowledge base of CTD, and PP2A subunit regulation
and toxic mechanism could be the frontiers of CTD.