ArticleHeliyon2022
Study on the molecular mechanisms of tetrandrine against pulmonary fibrosis based on network pharmacology, molecular docking and experimental verification.
Article in Heliyon, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Elucidating the Multi-Target Anti-Pruritic Mechanism ofCurrent issues in molecular biology · 2026Article
- Aronia Melanocarpa Elliot Anthocyanins Inhibits Alcoholic Liver Disease by Activation of α7nAChR.Plant foods for human nutrition (Dordrecht, Netherlands) · 2024Article
- Insights on exploring the therapeutic potential and structural modification of Tetrandrine.Future medicinal chemistry · 2024Review
- SPP1 promotes the polarization of M2 macrophages through the Jak2/Stat3 signaling pathway and accelerates the progression of idiopathic pulmonary fibrosis.International journal of molecular medicine · 2024Article
- Tetrandrine Alleviates Silica-induced Pulmonary Fibrosis Through PI3K/AKT Pathway: Network Pharmacology Investigation and Experimental Validation.Inflammation · 2024Article
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aims: This study aims to screen the potential targets of tetrandrine (Tet) against pulmonary fibrosis (PF) based on network pharmacological analysis, molecular docking and experimental verification. Main methods: The network pharmacology methods were employed to predict targets, construct Tet-PF-intersection target-pathway networks, and screen the candidate targets. The molecular docking was performed using AutoDockTools1.5.6. TGF-β1-induced human lung adenocarcinoma A549 cells were used as an Key findings: Six candidate targets were predicted based on network pharmacology and molecular docking, namely Significance: Combined with the results of theoretical calculation and experimental verification, and considering the roles of these targets in the pathogenesis of PF, Tet might antagonize PF by acting on
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Registered trials
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.