ArticleExperimental and therapeutic medicine2022
Chemerin promotes MAPK/ERK activation to induce inflammatory factor production in rat synoviocytes.
Article in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Molecular Basis of Adipose-Cardiac Crosstalk in Cardiovascular Diseases: From Mechanisms to Therapeutic Opportunities.Biomolecules · 2026Review
- Higenamine Hydrochloride Ameliorates Diabetic Cardiomyopathy Through RhoA/MEK/ERK Pathway.Inflammation · 2025Article
- MAPK Pathway Activation Patterns in the Synovium Reveal ERK1/2 and EGFR as Key Players in Osteoarthritis.Biomedicines · 2025Article
- Effect of adipokines on bone marrow mesenchymal stem cell function.World journal of stem cells · 2025Review
- Hand Osteoarthritis: Molecular Mechanisms, Randomized Controlled Trials, and the Future of Targeted Treatment.International journal of molecular sciences · 2025Review
- Signal Transduction Pathways Involved in Acupuncture-Mediated Inhibition of Synovitis in Knee Osteoarthritis: A Comprehensive Review.International journal of general medicine · 2025Review
- Obesity, Metabolic Syndrome, and Osteoarthritis-An Updated Review.Current obesity reports · 2023Review
- Beyond mechanical loading: The metabolic contribution of obesity in osteoarthritis unveils novel therapeutic targets.Heliyon · 2023Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemerin is a chemokine found in adipose tissue that specifically binds to the G protein-coupled receptor, chemokine-like receptor 1, and acts as a chemoattractant for macrophages and dendritic cells. Chemerin levels in the synovial fluid are associated with disease severity in patients with osteoarthritis (OA). However, to the best of our knowledge, the specific mechanism through which chemerin exerts its effects in OA remains unclear. The present study aimed to investigate the underlying mechanism of chemerin-associated synoviocyte inflammation. A Cell Counting Kit-8 assay was used to determine the optimal concentration of chemerin that exerted an effect on the viability of normal rat synoviocytes. The expression levels of MEK/ERK signaling pathway-related marker genes, including MEK, ERK, MMP-3 and MMP-13, were detected using reverse transcription-quantitative PCR. In addition, chemerin-induced phosphorylation of MEK, ERK1/2 and p38 MAPK was analyzed using western blotting, and the production of inflammatory factors following chemerin treatment was determined using ELISA. For the
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