ArticleJournal of bioenergetics and biomembranes2026
Mechanism of platelet-rich plasma inhibiting inflammatory response, oxidative stress, and senescence in synovial fibroblasts of patients with knee osteoarthritis via UBE2C based on transcriptome sequencing analysis.
Article in Journal of bioenergetics and biomembranes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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
1 citing paper in PubMed.
- Research landscape, hotspots, and evolutionary trends of knee osteoarthritis and oxidative stress: a multidimensional bibliometric analysis.Frontiers in medicine · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe incidence of knee osteoarthritis (KOA) continues to rise with the aging of the population, which seriously reduces the quality of life of patients. Platelet-rich plasma (PRP), a biological agent rich in growth factors and cytokines, has shown promising potential in the treatment of KOA in recent years. However, the specific molecular mechanism of its regulation of the pathological process is not clear.
methodsBased on the GSE157364 dataset, DESeq2 software was used to analyze the differentially expressed genes (DEGs) of OA-FLSs between the PRP group and the Ctrl group. KEGG pathway and GO function enrichment analysis were performed by SangerBox. The genes related to cell senescence, inflammatory response and oxidative stress were screened from the GeneCards database, and the intersection was obtained by a Venn diagram.
results911 DEGs (398 upregulated and 513 downregulated) were screened out. The expression of the key gene UBE2C in OA-FLSs was significantly downregulated compared with that in N-FLSs. PRP treatment significantly upregulated UBE2C expression in OA-FLSs, inhibited pro-inflammatory cytokine secretion, reduced intracellular ROS levels and β-Gal-positive senescent cell numbers, restored mitochondrial membrane potential, and downregulated the senescence-related proteins P21, P16, and P53.
conclusionPRP can inhibit the inflammatory response, oxidative stress injury, and cell senescence of OA-FLSs by upregulating the expression of UBE2C, thereby delaying the pathological process of KOA, which provides a new molecular target and theoretical basis for the clinical treatment of KOA.
Indexed as
Identifiers
41886168What OpenQuestion 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 OpenQuestion graph.