ArticleCartilage2021
High Mobility Group Box 1 Protein in Osteoarthritic Knee Tissue and Chondrogenic Progenitor Cells: An
Article in Cartilage, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Pondering the Potential of Hyaline Cartilage-Derived Chondroprogenitors for Tissue Regeneration: A Systematic Review.Cartilage · 2021Pooled it
- Cartilage Extracellular Matrix Homeostasis in Knee Osteoarthritis: Pathomechanisms and Therapeutic Targeting.Journal of cellular and molecular medicine · 2026Review
- DAMPs, PAMPs, and Alarmins: From Mechanism to Therapy.MedComm · 2026Review
- Article
- Mechanistic insights into non-coding RNAs regulate autophagy in chondrocytes and their contribution to osteoarthritis.Frontiers in medicine · 2025Review
- The Role of Alarmins in the Pathogenesis of Rheumatoid Arthritis, Osteoarthritis, and Psoriasis.Current issues in molecular biology · 2024Review
- Network Analysis of Osteoarthritis Progression Using a Steiner Minimal Tree Algorithm.Journal of inflammation research · 2024Article
- Effective Treatment of Knee Osteoarthritis Using a Nano-Enabled Drug Acupuncture Technology in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Achieving Nasal Septal Cartilage In Situ Regeneration: Focus on Cartilage Progenitor Cells.Biomolecules · 2023Review
- The Role of Alarmins in Osteoarthritis Pathogenesis: HMGB1, S100B and IL-33.International journal of molecular sciences · 2023Review
- The Triterpenoid Nrf2 Activator, CDDO-Me, Decreases Neutrophil Senescence in a Murine Model of Joint Damage.International journal of molecular sciences · 2023Article
- The Involvement of Neutrophils in the Pathophysiology and Treatment of Osteoarthritis.Biomedicines · 2022Review
- [Mechanism of high expression of high mobility group protein 1 in a rat model of knee osteoarthritis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- Enhancing the chondrogenic potential of chondrogenic progenitor cells by deleting RAB5C.iScience · 2021Article
- Relationship between the pyroptosis of fibroblast‑like synoviocytes and HMGB1 secretion in knee osteoarthritis.Molecular medicine reports · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIn osteoarthritis (OA), a loss of healthy cartilage extracellular matrix (ECM) results in cartilage degeneration. Attracting chondrogenic progenitor cells (CPCs) to injury sites and stimulating them toward chondrogenic expression profiles is a regenerative approach in OA therapy. High mobility group box 1 protein (HMGB1) is associated with chemoattractant and proinflammatory effects in various pathological processes. Here, we investigate the migratory effects of HMGB1 in knee OA and CPCs for the first time.
designImmunohistochemistry, immunoblotting, and immunocytochemistry were performed to identify HMGB1 and its receptors, receptor for advanced glycation end products (RAGE) and toll-like receptor 4 (TLR4) in OA knee tissue, chondrocytes, and CPCs. In situ hybridization for HMGB1 mRNA was performed in CPCs
resultsHMGB1 expression in OA tissue and OA chondrocytes was higher than in healthy specimens and cells. HMGB1, RAGE, and TLR4 were expressed in CPCs and chondrocytes. In situ hybridization revealed HMGB1 mRNA in CPCs after migration into OA knee tissue, and immunohistochemistry confirmed HMGB1 expression at the protein level. Stimulation via HMGB1 significantly increased the migration of CPCs.
conclusionsOur results show the chemoattractant role of HMGB1 in knee OA. HMGB1 is released by chondrocytes and has migratory effects on CPCs. These effects might be mediated via RAGE and TLR4. The
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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.