ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2020
MIR-140-5p affects chondrocyte proliferation, apoptosis, and inflammation by targeting HMGB1 in osteoarthritis.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.
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
41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 105 citations in OpenAlex.
- MicroRNAs in the diagnosis of osteoarthritis: a systematic review and meta-analysis of observational studies.Journal of orthopaedic surgery and research · 2025Pooled it
- MicroRNA expression in osteoarthritis: a meta-analysis.Clinical and experimental medicine · 2023Pooled it
- hsa_circ_0068631 facilitates the progression of diabetic retinopathy via regulating miR-140-5p in retinal microvascular endothelial cells.BMC ophthalmology · 2026Article
- Epigenetic regulation in osteoarthritis: recent updates and emerging mechanisms.Frontiers in genetics · 2026Review
- Current status and future prospects of nanocarrier-mediated miRNA delivery for osteoarthritis therapy.Frontiers in medicine · 2025Review
- Multi-omics analysis of small extracellular vesicles in osteoarthritis: bridging the gap between molecular insights and clinical applications.Burns & trauma · 2025Review
- The Role of MicroRNAs in the Pathophysiology of Osteoarthritis.International journal of molecular sciences · 2024Review
- microRNA-105-5p protects against chondrocyte injury, extracellular matrix degradation, and osteoarthritis progression by targeting SPARCL1.Histology and histopathology · 2024Article
- Inhibition of TLR4 signalling to dampen joint inflammation in osteoarthritis.Rheumatology (Oxford, England) · 2024Review
- Network Analysis of Osteoarthritis Progression Using a Steiner Minimal Tree Algorithm.Journal of inflammation research · 2024Article
- IRE1α regulates the PTHrP-IHH feedback loop to orchestrate chondrocyte hypertrophy and cartilage mineralization.Genes & diseases · 2024Article
- Mir-25-3p in extracellular vesicles from fibroblast-like synoviocytes alleviates pyroptosis of chondrocytes in knee osteoarthritis.Journal of bioenergetics and biomembranes · 2023Article
- Article
- The role of apoptosis in the pathogenesis of osteoarthritis.International orthopaedics · 2023Review
- The Role of Alarmins in Osteoarthritis Pathogenesis: HMGB1, S100B and IL-33.International journal of molecular sciences · 2023Review
- Hsa_circ_0007292 promotes chondrocyte injury in osteoarthritis via targeting the miR-1179/HMGB1 axis.Journal of orthopaedic surgery and research · 2023Article
- MicroRNA-140-5p inhibitor attenuates memory impairment induced by amyloid-ß oligomer in vivo possibly through Pin1 regulation.CNS neuroscience & therapeutics · 2023Article
- Research progress on the mechanism of interleukin-1β on epiphyseal plate chondrocytes.European journal of medical research · 2022Review
- Article
- New challenges for microRNAs in acute pancreatitis: progress and treatment.Journal of translational medicine · 2022Review
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 at 3 institutions in 1 country.
Funding
Abstract
objectiveThis study aimed to test the expression and biological function of miR-140-5p in osteoarthritis (OA), and identify its target gene and explore its mechanism in OA.
methodsDifferential genes were screened and analyzed by gene microarray and WGCNA analysis. The normal human chondrocytes C28/I2 were induced by IL-1β to construct the OA cell model. The expression of miR-140-5p and high mobility group box 1 (HMGB1) was quantified by quantitative real-time PCR (qRT-PCR) in OA tissues and IL-1β-induced chondrocytes. Western blotting was performed to evaluate the expression of HMGB1 and PI3K/AKT pathway activation. The concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-6, MMP-1 and MMP-3 were determined by ELISA. CCK-8 and flow cytometry were conducted to determine the cellular capabilities of proliferation and cell apoptosis.
resultsBioinformatics analysis demonstrated that HMGB1 was highly expressed in OA and activated PI3K/AKT pathway. Also, HMGB1 was predicted as a target of miR-140-5p. The levels of miR-140-5p were negatively correlated with HMGB1 in OA tissues and IL-1β-induced chondrocytes. The overexpression of miR-140-5p reduced the expression of HMGB1 protein, p-AKT (Ser473) and p-PI3K in IL-1β-induced chondrocytes. Besides, the expression of p-AKT (Ser473) and p-PI3K was significantly upregulated by employing miR-140-5p inhibitor, but retrieved after treating with LY294002. Furthermore, miR-140-5p inhibited inflammation, matrix metalloprotease expression and apoptosis in IL-1β-induced chondrocytes through regulating HMGB1.
conclusionMiR-140-5p was down-regulated while HMGB1 was upregulated in OA. MiR-140-5p could inhibit the PI3K/AKT signaling pathway and suppress the progression of OA through targeting HMGB1.
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.