Evidence map›Paper›PMID 37087476›Full record

ArticleJournal of orthopaedic surgery and research2023

Network pharmacology identifies fisetin as a treatment for osteoporosis that activates the Wnt/β-catenin signaling pathway in BMSCs.

Guihong Liang, Jinlong Zhao, Jianke Pan, Yuan Yang, Yaoxing Dou, Weiyi Yang, Lingfeng Zeng, Jun Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of orthopaedic surgery and research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. International journal of molecular sciences · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Guihong Liang *The Second Clinical Medical College of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.ORCID http://orcid.org/0000-0002-7599-2628
Jinlong Zhao *The Second Clinical Medical College of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.ORCID http://orcid.org/0000-0001-7079-1336
Jianke PanThe Second Affiliated Hospital of Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, 510120, China.ORCID http://orcid.org/0000-0002-4596-6111
Yuan YangThe Second Clinical Medical College of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Yaoxing DouThe Second Clinical Medical College of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Weiyi YangThe Second Affiliated Hospital of Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, 510120, China.ORCID http://orcid.org/0000-0001-8657-2269
Lingfeng ZengThe Second Clinical Medical College of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China. lingfengzeng@gzucm.edu.cn.ORCID http://orcid.org/0000-0003-1311-8641
Jun LiuThe Research Team on Bone and Joint Degeneration and Injury of Guangdong Provincial Academy of Chinese Medical Sciences, Guangzhou, 510120, China. gzucmliujun@foxmail.com.ORCID http://orcid.org/0000-0002-1943-3880
Guangzhou University of Chinese Medicine · CN

Funding

Guangdong Basic and Applied Basic Research Foundation 2022A1515010385Guangdong Basic and Applied Basic Research Foundation 2022A1515011700Guangdong Basic and Applied Basic Research Foundation 2022A1515220131Guangdong Basic and Applied Basic Research Foundation 2023A1515012626Project of Philosophy and Social Science Planning of Guangzhou 2022GZQN42Research Fund for Bajian Talents of Guangdong Provincial Hospital of Chinese Medicine BJ2022KY01Science and Technology Program of Guangzhou 202102010273Science and Technology Program of Guangzhou 2023A03J0238the National key research and development program 2021YFC1712804the National Natural Science Foundation of China No. 81974574the National Natural Science Foundation of China No.82004383
6 · The paper itself

Abstract

backgroundAlthough fisetin may exist widely in many natural herbs, its anti-OP mechanism is still unclear. The aim of this study is to explore the molecular anti-osteoporosis (OP) mechanism of fisetin based on network pharmacology and cell experiments.

methodsThe target of fisetin was extracted by the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP). The targets of OP were obtained by DisGeNET, GeneCards and the Comparative Toxicogenomics Database, and the targets of fisetin in OP were screened by cross-analysis. The protein-protein interaction (PPI) network was constructed by STRING, and the core targets were obtained. We performed gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses on common targets via the Database for Annotation, Visualization and Integrated Discovery. Finally, an in vitro cell experiment was used to verify the anti-OP effect and mechanism of fisetin.

resultsThere are 44 targets of fisetin related to the treatment of OP. The PPI results suggest that CTNNB1, CCND1, TP53, JUN, and AKT1 are the core targets. A total of 259 biological process, 57 molecular function and 26 cell component terms were obtained from GO enrichment analysis. The results of KEGG pathway enrichment analysis suggested that fisetin treatment of OP may be related to the Wnt signaling pathway, estrogen signaling pathway, PI3K-Akt signaling pathway and other signaling pathways. In vitro cell experiments showed that fisetin significantly increased the expression levels of ALP, collagen I, osteopontin and RUNX2 in bone marrow mesenchymal stem cells (BMSCs) (p < 0.05). Fisetin also increased the gene expression levels of Wnt3 and β-catenin (CTNNB1) in BMSCs, which indicates that fisetin can regulate the Wnt/β-catenin signaling pathway and promote the osteogenic differentiation of BMSCs.

conclusionsFisetin acts on multiple targets and pathways in the treatment of OP; mechanistically, it regulates the Wnt/β-catenin signaling pathway, which promotes the osteogenic differentiation of BMSCs and maintains bone homeostasis. The results of this study provide a theoretical basis for further study on the complex anti-OP mechanism of fisetin.

Indexed as

Drugs, Chinese HerbalFlavonolsNetwork PharmacologyOsteoporosisWnt Signaling PathwayMesenchymal Stem CellsOsteogenesisPhosphatidylinositol 3-KinasesDrugs, Chinese HerbalfisetinFlavonolsPhosphatidylinositol 3-KinasesBMSCsBone homeostasisChinese traditional medicineFisetinMechanismsOsteoporosis

Identifiers

PMID37087476
PMCPMC10122799
OpenAlexW4366768301

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.