ArticlePloS one2016
Effects of UCP4 on the Proliferation and Apoptosis of Chondrocytes: Its Possible Involvement and Regulation in Osteoarthritis.
Article in PloS one, 2016. 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 It has been retracted, and should not be counted.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 9 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
9 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- MFN2 deficiency affects calcium homeostasis in lung adenocarcinoma cells via downregulation of UCP4.FEBS open bio · 2023Article
- Mitochondrial Uncoupling Proteins (UCPs) as Key Modulators of ROS Homeostasis: A Crosstalk between Diabesity and Male Infertility?Antioxidants (Basel, Switzerland) · 2021Review
- miR-335-5P contributes to human osteoarthritis by targeting HBP1.Experimental and therapeutic medicine · 2021Article
- BNIP3 decreases the LPS-induced inflammation and apoptosis of chondrocytes by promoting the development of autophagy.Journal of orthopaedic surgery and research · 2020Article
- Mitochondrial Uncoupling Proteins: Subtle Regulators of Cellular Redox Signaling.Antioxidants & redox signaling · 2018Review
- Influence of protein kinase RIPK4 expression on the apoptosis and proliferation of chondrocytes in osteoarthritis.Molecular medicine reports · 2018Article
- Electroacupuncture serum inhibits TNF‑α‑mediated chondrocyte inflammation via the Ras‑Raf‑MEK1/2‑ERK1/2 signaling pathway.Molecular medicine reports · 2017Article
- Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis.International journal of molecular sciences · 2016Review
Corrections and comments
- Retraction · 2025-05-07Concerns/Issues about Animal Welfare · Concerns/Issues about Image · Duplication of/in Image · Euphemisms for Duplication · Original Data and/or Images not Provided and/or not Available · Results Not Reproducible · · See also: https://pubpeer.com/publications/64BCDFD8993FA252D214404457C7D6
- Retracted
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS)-induced chondrocytes apoptosis plays a key role in osteoarthritis (OA) pathogenesis. Uncoupling protein 4 (UCP4) can protect cells against oxidative stress via reducing ROS production and cell apoptosis. Here, silencing of UCP4 in primary chondrocytes significantly inhibited cell survival, but induced ROS production and cell apoptosis. UCP4 mRNA of cartilage tissues was decreased in osteoarthritis patients, which was negatively correlated with synovial fluid (SF) leptin concentration. Moreover, leptin treatment (5, 10 and 20 ng/ml) of primary cultured chondrocytes significantly decreased mRNA and protein levels of UCP4, but increased ROS production and cell apoptosis in a dose-dependent manner. The effects of leptin treatment (20 ng/ml) on chondrocytes was partially reversed by ectopic expression of UCP4. More importantly, intraarticularly injection of UCP4 adenovirus remarkably alleviate OA progression and cell apoptosis in a rat OA model induced by anterior cruciate ligament transection (ACLT). In conclusion, UCP4, whose expression was suppressed by leptin, may be involved in the ROS production and apoptosis of chondrocytes, thus contributing to the OA pathogenesis.
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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.