ArticleHereditas2025
Identification of CD36 as a contributor in inflammatory response of rheumatoid arthritis and screening of feasible bioactive drugs targeting it.
Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Immune responses in aging adults.The Journal of clinical investigation · 2026Review
- Investigation of complex miRNA-mRNA interaction networks during JAK inhibitor therapy in rheumatoid arthritis.Frontiers in pharmacology · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRheumatoid arthritis (RA) is a chronic inflammatory disease. This study aims to identify candidate therapeutic targets and promising drugs for RA.
methodsRA-related microarray datasets (GSE77298 and GSE206848) and inflammatory genes (IRGs) were downloaded from Gene Expression Omnibus database and GeneCards database, respectively. After removing batch effects, differentially expressed genes (DEGs) were screened using filtering criteria of P < 0.05 and |log2(fold change)|> 1. Differentially expressed IRGs (DE-IRGs) were then obtained. Key gene modules were identified by weighted gene co-expression network analysis (WGCNA), and the hub genes were then identified from the results of protein-protein interaction (PPI) network analysis, WGCNA and DE-IRGs, and validated by a external dataset GSE93272. Receiver operating characteristic (ROC) curve was used to evaluate the diagnostic effect of the predicted hub genes. In addition, drug prediction was performed through virtual screening. mRNA and protein expression of cluster of differentiation 36 (CD36) were detected by RT-qPCR and Western blot. After RA fibroblast-like synovial cells (RA-FLS) were treated with piceatannol and epicatechin, cell proliferation was detected by CCK-8 assay, and flow cytometry was used to detect cell cycle and apoptosis, and the secretion of inflammatory cytokines was detected by enzyme-linked immunosorbent assay.
resultsThree hub genes were finally identified, including CD36, perilipin 1 and lipoprotein lipase. CD36 was further identified as a candidate biomarker and therapeutic target for RA, which had relatively good diagnostic efficacy for RA. Compared with fibroblast-like synovial cells (FLS), mRNA and protein expression levels of CD36 in RA-FLS were significantly up-regulated (P < 0.05). Piceatannol and epicatechin had good binding affinity with CD36 (docking score < -5 kcal/mol), and piceatannol treatment or epicatechin treatment inhibited the proliferation and inflammation of RA-FLS and induced cell cycle arrest and apoptosis (P < 0.05).
conclusionCD36 is a potential biomarker and therapeutic target associated with synovial inflammation of RA, and piceatannol and epicatechin are potential natural drugs for RA treatment. Overall, these findings provide new insights into the clinical diagnosis and treatment of RA.
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