ArticleGene therapy2019
Inhibition of microRNA-495 suppresses chondrocyte apoptosis through activation of the NF-κB signaling pathway by regulating CCL4 in osteoarthritis.
Article in Gene therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 25 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- Programmed cell death in osteoarthritis.Apoptosis : an international journal on programmed cell death · 2026Review
- Identification and functional analysis of hub genes in knee osteoarthritis via bioinformatics and experimental validation.Frontiers in bioinformatics · 2025Article
- The Causal Effects Between Circulating Inflammatory Proteins and Osteoarthritis: A Mendelian Randomization and Transcriptomic Analysis.Journal of pain research · 2025Article
- Natural products in osteoarthritis treatment: bridging basic research to clinical applications.Chinese medicine · 2024Review
- Chemokines in Cartilage Regeneration and Degradation: New Insights.International journal of molecular sciences · 2023Review
- Bioinformatics and system biology analysis revealed the crosstalk between COVID-19 and osteoarthritis.Immunity, inflammation and disease · 2023Article
- Gene augmentation for autosomal dominant retinitis pigmentosa using rhodopsin genomic loci nanoparticles in the P23HGene therapy · 2023Article
- CC chemokines and receptors in osteoarthritis: new insights and potential targets.Arthritis research & therapy · 2023Review
- Recent Therapeutic Strategies for Excessive Chondrocyte Death in Osteoarthritis: A Review.Orthopaedic surgery · 2023Review
- Association between an Increased Serum CCL5 Level and Pathophysiology of Degenerative Joint Disease in the Temporomandibular Joint in Females.International journal of molecular sciences · 2023Article
- Soluble and EV-Associated Diagnostic and Prognostic Biomarkers in Knee Osteoarthritis Pathology and Detection.Life (Basel, Switzerland) · 2023Review
- Ameliorative Effects of Peptide Phe-Leu-Ala-Pro on Acute Liver and Kidney Injury Caused by CClACS omega · 2022Article
- Sepsis induces variation of intestinal barrier function in different phase through nuclear factor kappa B signaling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021Article
- Downregulation of MicroRNA-495 Alleviates IL-1β Responses among Chondrocytes by Preventing SOX9 Reduction.Yonsei medical journal · 2021Article
- Review
- CircSNHG5 Sponges Mir-495-3p and Modulates CITED2 to Protect Cartilage Endplate From Degradation.Frontiers in cell and developmental biology · 2021Article
- CircSERPINE2 weakens IL-1β-caused apoptosis and extracellular matrix degradation of chondrocytes by regulating miR-495/TGFBR2 axis.Bioscience reports · 2020Article
- [Regulation of long non-coding RNA in cartilage injury of osteoarthritis].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2020Article
- Expression of miR-495 and miR-326 in peripheral blood of rheumatoid arthritis patients and its significance.Experimental and therapeutic medicine · 2020Article
- Neferine Inhibits Expression of Inflammatory Mediators and Matrix Degrading Enzymes in IL-1β-Treated Rat Chondrocytes via Suppressing MAPK and NF-κB Signaling Pathways.Inflammation · 2020Article
Corrections and comments
- Retraction · 2024-09-09Concerns/Issues about Data · Concerns/Issues about Image · Investigation by Journal/Publisher · Unreliable Data · · see lso: https://pubpeer.com/publications/A9E47EDC98D857B78D5EEB6CCF2F81
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a common form of arthritis, osteoarthritis (OA) represents a degenerative disease, characterized by articular cartilage damage and synovium inflammation. Recently, the role of various microRNAs (miRs) and their specific expression in OA has been highlighted. Therefore, the aim of the current study was to elucidate the role by which miR-495 and chemokine ligand 4 (CCL4) influence the development and progression of OA. OA mice models were established, after which the CCL4 and collagen levels as well as cell apoptosis were determined in cartilage tissue of OA mice. The chondrocytes of the OA mice models were subsequently treated with a series of miR-495 mimic, inhibitor, and siRNA against CCL4. Afterwards, miR-495 expressions as well as the levels of CCL4, p50, p65, and IkBa and the extent of IkBa phosphorylation in addition to the luciferase activity of NF-kB were measured accordingly. Finally, cell apoptosis and cell cycle distribution were detected. miR-495 was highly expressed while NF-κB, CCL4, and collagen II were poorly expressed. Cell apoptosis was elevated in the cartilage tissue of the OA mice. CCL4 was a potential target gene of miR-495. Downregulation of miR-495 led to accelerated chondrocyte proliferation accompanied by diminished cell apoptosis among the OA mice. Taken together, the results of the current study demonstrated that inhibition of miR-495 suppressed chondrocyte apoptosis and promoted its proliferation through activation of the NF-κB signaling pathway by up-regulation of CCL4 in OA.
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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.