ArticleCentral-European journal of immunology2024
LncRNA RMRP promotes chondrocyte injury by regulating the FOXC1/RBP4 axis.
Article in Central-European journal of immunology, 2024. 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
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
2 citing papers in PubMed.
- Y-box binding protein 1 stabilizes EP300 mRNA and promotes forkhead box C1 H3K27Ac to aggravate chondrocyte injury in osteoarthritis.Journal of cell communication and signaling · 2025Article
- RNA Polymerase III-Transcribed RNAs in Health and Disease: Mechanisms, Dysfunction, and Future Directions.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: The main pathological feature of osteoarthritis (OA) is chondrocyte injury. LncRNA mitochondrial RNA processing endoribonuclease (RMRP) has been shown to be a chondrogenic differentiation factor. This study aimed to explore the role of RMRP in chondrocyte injury. Material and methods: Cell counting kit-8 (CCK-8) and TUNEL assays were used to determine lipopolysaccharide (LPS)-induced chondrocyte viability and apoptosis, respectively. The interaction between RMRP and FOXC1 was analyzed by RIP and RNA pull-down. Dual luciferase reporter and ChIP were employed to analyze the interaction between FOXC1 and RBP4. The levels of RMRP, FOXC1, RBP4, apoptosis-related and extracellular matrix (ECM)-related genes were detected by RT-qPCR and western blot. ELISA assay was used for detection of inflammatory cytokines in LPS-induced chondrocytes. Results: The levels of RMRP, FOXC1 and RBP4 were significantly upregulated in OA cartilage tissues and LPS-induced chondrocytes. Knockdown of RMRP inhibited chondrocyte apoptosis and inflammation under LPS. RMRP interacted with FOXC1 and promoted RBP4 expression. FOXC1 could upregulate RBP4 and promote LPS-induced chondrocyte apoptosis and inflammation. Similarly, RMRP combined with FOXC1 and aggravated apoptosis and inflammation in LPS-treated chondrocytes. Conclusions: RMRP promoted upregulation of RBP4 and activation of the JNK signaling pathway by binding to FOXC1, thereby accelerating LPS-induced apoptosis and inflammation in chondrocytes.
Indexed as
Identifiers
What 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.