ArticleInternational journal of molecular medicine2024
Unveiling the role of RhoA and ferroptosis in vascular permeability: Implications for osteoarthritis.
Article in International journal of molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- RhoA deficiency in chondrocyte inhibits cartilage fibrosis and ameliorates osteoarthritis progression via SOX4/MMP2 axis.Journal of orthopaedic translation · 2026Article
- Brief pulses of high-level fluid shear stress enhance metastatic potential and rapidly alter the metabolism of cancer cells.Cell reports · 2026Article
- Synovial macrophage rhoa protects against osteoarthritis by suppressing YAP/IL-17C mediated chondrocyte senescence.Cell biology and toxicology · 2026Article
- The role of ferroptosis in vascular endothelial cells and its role in the pathogenesis of cervical spondylosis of vertebral artery type: a comprehensive review.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026Review
- Potential crosstalk between ferroptosis and immunosenescence in osteoarthritis: evidence integration and translational insights from the osteoimmune microenvironment.Frontiers in immunology · 2026Review
- Regulation of H-type angiogenesis and permeability in the subchondral bone of osteoarthritis: the role of Slit3 and the Robo4/Rac1-GTP/ROS axis.Frontiers in cell and developmental biology · 2026Article
- Iron-dependent ferroptosis in cardiac microvascular endothelial cells: a key link between dysregulated iron homeostasis and microcirculatory injury during myocardial ischemia-reperfusion.Frontiers in cardiovascular medicine · 2026Review
- Tcirg1 deficiency delays osteoarthritis progression by impairing lysosome acidification and peripheral accumulation in osteoclasts.Frontiers in cell and developmental biology · 2025Article
- Ferroptosis in osteoarthritis: metabolic reprogramming, immunometabolic crosstalk, and targeted intervention strategies.Frontiers in immunology · 2025Review
- Osteoarthritis as a clinical marker of cardiovascular-kidney-metabolic multimorbidity: a population-based cohort study in China.Frontiers in endocrinology · 2025Article
- Ferroptosis-related genes and pathways in knee osteoarthritis cartilage degeneration: discovered by bioinformatics technology and in vivo experimental verification.American journal of translational research · 2025Article
Corrections and comments
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal angiogenesis and increased vascular permeability of subchondral bone are key mechanisms related to osteoarthritis (OA). However, the precise mechanisms responsible for heightened vascular permeability in OA remain unclear. The present study used proteomics to identify protein expression in damaged subchondral bone compared with normal subchondral bone. The results suggest that Ras homolog family member A (RhoA) may be associated with the vascular permeability of subchondral bone and ferroptosis in OA. The results of analysis of clinical samples indicated a significant increase in expression of RhoA in the subchondral bone of OA. This were consistent with the proteomics findings. We found through western blotting, RT‑PCR, and immunofluorescence that RhoA significantly increased the permeability of endothelial cells (ECs) by inhibiting inter‑EC adhesion proteins (zona occludens‑1, connexin 43 and Vascular endothelial‑Cadherin) and actin filaments. Furthermore, RhoA induced ferroptosis core proteins (glutathione peroxidase 4, solute carrier family 7 member 11 and acyl‑CoA synthase long‑chain family member 4, ACSL4) by influencing lipid peroxidation and mitochondrial function, leading to ferroptosis of ECs. This suggested an association between RhoA, ferroptosis and vascular permeability. Ferroptosis significantly increased permeability of ECs by inhibiting inter‑EC adhesion proteins. RhoA increased vascular permeability by inducing ferroptosis of ECs.
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