ArticleCell death & disease2019
CEMIP (KIAA1199) induces a fibrosis-like process in osteoarthritic chondrocytes.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 2 of them syntheses that pooled it.
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Who cites it
59 citing papers in PubMed, 2 syntheses or guidelines pooled it, 91 citations in OpenAlex.
- Cross-species transcriptome-wide meta-analysis of anterior cruciate ligament rupture.BMC genomics · 2025Pooled it
- Pooled it
- ADSC-enriched adipose extract alleviates cartilage fibrosis in temporomandibular joint osteoarthritis by inhibiting chondrocyte senescence.Journal of translational medicine · 2025Trial
- SERPINE1/PAI-1 in Skeletal Degeneration: A Proposed Context-Dependent Framework for Bone Remodeling Regulation.Calcified tissue international · 2026Review
- Artemotil Attenuates Fibrosis-Associated Chondrocyte Remodelling in Osteoarthritis in Association With STC1-Related TGF-β/SMAD2/3 Signalling.Journal of cellular and molecular medicine · 2026Article
- Spatial and functional characterization of ER stress proteins links fibroblast plasticity and proliferative processes in human osteoarthritic synovitis.Cell death and differentiation · 2026Article
- Cell migration inducing protein alleviates adverse cardiac remodelling after ischaemia and reperfusion injury by controlling fibroblast activation.Cardiovascular research · 2026Article
- KIAA1199 aggravates sepsis-induced lung injury by promoting complement activation.Communications biology · 2026Article
- RhoA deficiency in chondrocyte inhibits cartilage fibrosis and ameliorates osteoarthritis progression via SOX4/MMP2 axis.Journal of orthopaedic translation · 2026Article
- Acupotomy Ameliorates Articular Cartilage Fibrosis in a Rabbit Model of Knee Osteoarthritis via the TGF-β1/Smad Pathway.Orthopedic research and reviews · 2026Article
- Pirfenidone Attenuates Fibrosis and Neovascularization in 3D Spheroid-Laden Hydrogel Culture.Journal of tissue engineering and regenerative medicine · 2026Article
- Multi-scale integration of human brain vascular and CSF proteomes reveals biomarkers of cerebral amyloid angiopathy linked to Alzheimer's disease risk.medRxiv : the preprint server for health sciences · 2025Article
- Review
- CEMIP Maintains Vascular Contractility by Controlling PP1c-MLC20 Cascade in SMCs.Circulation research · 2025Article
- M2-like macrophages derived from THP-1 cells promote myofibroblast differentiation of synovial fibroblasts in association with the TGF-β1/SMAD2/3 signaling pathway.Scientific reports · 2025Article
- Andrographolide suppresses fibrogenic phenotype of chondrocytes and ameliorates osteoarthritis by regulating miR-137/BMP7 axis.Journal of orthopaedics · 2025Article
- Hyaluronan-Binding Protein Promotes Fibroblast Transformation and Heart Failure by Modulating the STAT5A-MMP13 Pathway.Biomedicines · 2025Article
- Upregulated CEMIP promotes intervertebral disc degeneration via AP-1-mediated change in chromatin accessibility.Clinical and translational medicine · 2025Article
- Fibrocartilage hyalinization: A potential therapeutic strategy for articular fibrocartilage.Journal of orthopaedic translation · 2025Review
- circ_0002970 promotes fibroblast-like synoviocytes invasion and the inflammatory response through Hippo/YAP signaling to induce CTGF/CCN1 expression in rheumatoid arthritis.Arthritis research & therapy · 2025Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CEMIP (for "Cell migration-inducing protein" also called KIAA1199 and Hybid for "Hyaluronan-binding protein") expression is increased in cancers and described as a regulator of cell survival, growth and invasion. In rheumatoid arthritis, CEMIP is referred to as an angiogenic marker and participates in hyaluronic acid degradation. In this study, CEMIP expression is investigated in healthy and osteoarthritis (OA) cartilage from human and mouse. Its role in OA physiopathology is deciphered, specifically in chondrocytes proliferation and dedifferentiation and in the extracellular matrix remodeling. To this end, CEMIP, αSMA and types I and III collagen expressions were assessed in human OA and non-OA cartilage. CEMIP expression was also investigated in a mouse OA model. CEMIP expression was studied in vitro using a chondrocyte dedifferentiation model. High-throughput RNA sequencing was performed on chondrocytes after CEMIP silencing. Results showed that CEMIP was overexpressed in human and murine OA cartilage and along chondrocytes dedifferentiation. Most of genes deregulated in CEMIP-depleted cells were involved in cartilage turnover (e.g., collagens), mesenchymal transition and fibrosis. CEMIP regulated β-catenin protein level. Moreover, CEMIP was essential for chondrocytes proliferation and promoted αSMA expression, a fibrosis marker, and TGFβ signaling towards the p-Smad2/3 (Alk5/PAI-1) pathway. Interestingly, CEMIP was induced by the pSmad1/5 (Alk1) pathway. αSMA and type III collagen expressions were overexpressed in human OA cartilage and along chondrocytes dedifferentiation. Finally, CEMIP was co-expressed in situ with αSMA in all OA cartilage layers. In conclusion, CEMIP was sharply overexpressed in human and mouse OA cartilage and along chondrocytes dedifferentiation. CEMIP-regulated transdifferentiation of chondrocytes into "chondro-myo-fibroblasts" expressing α-SMA and type III collagen, two fibrosis markers. Moreover, these "chondro-myo-fibroblasts" were found in OA cartilage but not in healthy cartilage.
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