ArticlePloS one2026
Network pharmacology and integrative bioinformatics analyses identify PDE1A as a key target of pirfenidone in idiopathic pulmonary fibrosis.
Article in PloS one, 2026. 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
Pirfenidone, an antifibrotic agent, has been shown to be effective in the treatment of idiopathic pulmonary fibrosis (IPF). However, the exact mechanism of action and clinical efficacy require further investigation and validation. This study commenced by identifying pathogenic genes associated with IPF through the GeneCards database. Potential targets of pirfenidone were subsequently screened through PubChem and Swiss TargetPrediction, and overlapping targets were identified through Venn diagram analysis. Enrichment analysis of potential target genes was performed to identify the key biological processes and pathways involved in the action of pirfenidone. The main target genes were subsequently identified through the GSE10667 and GSE110147 datasets. The affinity of PDE1A to pirfenidone was predicted by molecular docking and MicroScale Thermophoresis (MST). Finally, the expression and antifibrotic effects of pirfenidone on PDE1A were validated through data from the GSE226249 dataset. PDE1A, identified by GeneCards and Swiss TargetPrediction, was found to be an important mediator of the antifibrotic effect of pirfenidone. The enrichment analysis revealed biological processes such as cyclic nucleotide-mediated signaling and cAMP-mediated signaling. KEGG pathway analysis further linked pirfenidone activity to pathways involved in calcium signaling, taste transduction, morphine dependence, renin secretion and purine metabolism. Molecular docking, molecular dynamics (MD) simulations and MST results revealed a strong binding affinity between pirfenidone and PDE1A. MD simulations showed the stability of the complex. It was observed that the RMSD analysis of the complex stabilized between 0.6 to 0.8 nm throughout the simulation, however RMSF showed minimal fluctuation. Data from the GSE226249 dataset confirmed that upregulation of PDE1A promotes fibrosis, whereas pirfenidone downregulates PDE1A, thereby exerting its antifibrotic effect. The inhibition of IPF progression by pirfenidone is mediated by PDE1A, providing insights into its therapeutic mechanism.
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.