ArticleAnimal models and experimental medicine2024
The decrease in zinc-finger E-box-binding homeobox-1 could accelerate steroid-induced osteonecrosis of the femoral head by repressing type-H vessel formation via Wnt/β-catenin pathway.
Article in Animal models and experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed.
- Recent advances in glucocorticoid regulation of bone and the bone marrow niche: Genetic and pharmacological approaches to understand and prevent bone loss.Current opinion in endocrine and metabolic research · 2026Article
- A migrasome-based osteoinductive strategy: reprogramming the bone microenvironment for accelerated coupling of angiogenesis and osteogenesis.Journal of nanobiotechnology · 2026Article
- ZEB1 maintains mitochondrial fission and macrophage efferocytosis by restraining MFN2, thereby limiting inflammation and improving tendon‑bone healing.International journal of molecular medicine · 2026Article
- Single-cell RNA sequencing analysis reveals the evolution and regulatory features of specialized endothelial cell subsets in non-traumatic osteonecrosis of the femoral head.Biology direct · 2026Article
- Targeting type H vessels with bioactive metabolites from traditional Chinese botanical drugs: a therapeutic strategy for skeletal disorders.Frontiers in pharmacology · 2025Review
- The decrease in zinc-finger E-box-binding homeobox-1 could accelerate steroid-induced osteonecrosis of the femoral head by repressing type-H vessel formation via Wnt/β-catenin pathway.Animal models and experimental medicine · 2024Article
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Abstract
backgroundZinc-finger E-box-binding homeobox-1 (ZEB1) is predominantly found in type-H vessels. However, the roles of ZEB1 and type-H vessels in steroid-induced osteonecrosis of the femoral head (SONFH) are unclear.
methodsHuman femoral heads were collected to detect the expression of ZEB1 and the levels of type-H vessels. Then, the SONFH model was developed by injecting C57BL/6 mice with lipopolysaccharide and methylprednisolone. Micro-computed tomography, angiography, double calcein labeling, immunofluorescence, immunohistochemistry, quantitative real-time polymerase chain reaction, and Western blotting were performed to detect the expression of ZEB1, the Wnt/β-catenin pathway, type-H vessels, and the extent to which ZEB1 mediates angiogenesis and osteogenesis. Human umbilical vein endothelial cells were also used to explore the relationship between ZEB1 and the Wnt/β-catenin pathway.
resultsWe found that ZEB1 expression and the formation of type-H vessels decreased in SONFH patients and in a mouse model. The number of vascular endothelial growth factors in the femoral heads also decreased. Moreover, the bone mineral density, trabecular number, mineral apposition rate, and expression of genes related to osteogenesis decreased. After ZEB1 knockdown, angiogenesis and osteogenesis decreased. However, the numbers of type-H vessels and the extent of angiogenesis and osteogenesis improved after activation of the Wnt/β-catenin pathway.
conclusionsThe ZEB1 expression decreased in SONFH, causing a decrease in type-H vessel, and it mediated angiogenesis and osteogenesis by regulating the Wnt/β-catenin pathway, ultimately accelerating the process of SONFH.
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