ArticleNarra J2025
In silico studies on quercetin, myricetin, and kaempferol in inhibiting TGF-β1 and galectin- 3 for cardiac fibrosis management.
Article in Narra J, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac fibrosis remains as the leading cause of death worldwide and is often associated with elevated levels of transforming growth factor-β 1 (TGF-β1) and galectin-3, making them potential therapeutic targets. Recent studies revealed that quercetin, myricetin, and kaempferol have the biological effect for several cardiovascular diseases. However, the investigation into this topic through molecular models and analysis remain unexplored. The aim of this study was to evaluate the potential effect of quercetin, myricetin, and kaempferol which targeted TGF-β1 and galectin-3. In this study, quercetin, myricetin, and kaempferol roled as the tested ligands. Subsequently, colchicine and native ligand acted as control ligands that were screened through molecular docking against TGF-β1 and galectin-3 using AutoDock tools to identify the potential inhibitor. The stability of ligand- receptor complexes was assessed through molecular dynamic (MD) simulations using NMAD. Absorption, Distribution, Metabolism, Excretion and toxicity (ADMET) prediction were also performed using ADMETlab 2.0. Molecular docking analysis revealed that quercetin, myricetin, and kaempferol exhibited strong binding affinity which are -8.9 kcal/mol, -8.5 kcal/mol, -7.6 kcal/mol respectively with TGF-β1, and -7.5 kcal/mol, -7.0 kcal/mol, -5.7 kcal/mol respectively with galetcin-3; low inhibition constant (Ki); and stable interaction with the active sites of TGF-β1 and galectin-3. MD simulations confirmed the stability and compactness of the ligand-receptor complexes. ADMET analysis also showed high Plasma Protein Binding (PPB) values (quercetin: 95%, myricetin: 92%, and kaempferol: 97%) and moderate clearance values (quercetin: 8.284%, myricetin, and 7.716%, kaempferol: 6.868%) for the tested compounds. In conclusion, the in silico analyses suggested that quercetin, myricetin, and kaempferol are promising for cardiac fibrosis therapies by inhibiting TGF-β1 and galectin-3.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.