ArticleHeliyon2024
CHRDL2 activates the PI3K/AKT pathway to ameliorate glucocorticoid-induced damages to bone microvascular endothelial cells (BMECs).
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed.
- Endothelial Responses to ICS/LABA Combinations Are Determined Primarily by the Corticosteroid Component.International journal of molecular sciences · 2026Article
- Human Umbilical Cord Mesenchymal Stem Cells Protect Against Steroid-Induced Osteonecrosis of the Femoral Head Through Hippo Pathway.Biomedicines · 2026Article
- The role of post-translational modifications in osteonecrosis of the femoral head.Frontiers in cell and developmental biology · 2026Review
- Serum DLX6-AS1 and miR-141-3p as early diagnostic biomarkers and regulators of delayed fracture healing (DFH).Journal of orthopaedic surgery and research · 2025Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Steroid-induced avascular necrosis of the femoral head (ANFH) is characterized by the death of bone tissues, leading to the impairment of normal reparative processes within micro-fractures in the femoral head. Glucocorticoid (GCs)-induced bone microvascular endothelial cell (BMEC) damage has been reported to contribute to ANFH development. In this study, differentially expressed genes (DEGs) between necrosis of the femoral head (NFH) and normal samples were analyzed based on two sets of online expression profiles, GSE74089 and GSE26316. Chordin-like 2 (CHRDL2) was found to be dramatically downregulated in NFH samples. In GCs-stimulated BMECs, cellular damages were observed alongside CHRDL2 down-regulation. GCs-caused cell viability suppression, cell apoptosis promotion, tubule formation suppression, and cell migration suppression were partially abolished by CHRDL2 overexpression but amplified by CHRDL2 knockdown; consistent trends were observed in GCs-caused alterations in the protein levels of VEGFA, VEGFR2, and BMP-9 levels, and the ratios of Bax/Bcl-2 and cleaved-caspase3/Caspase3. GC stimulation significantly inhibited PI3K and Akt phosphorylation in BMECs, whereas the inhibitor effects of GCs on PI3K and Akt phosphorylation were partially attenuated by CHRDL2 overexpression but further amplified by CHRDL2 knockdown. Moreover, CHRDL2 overexpression caused improvement in GCs-induced damages to BMECs that were partially eliminated by PI3K inhibitor LY294002. In conclusion, CHRDL2 is down-regulated in NFH samples and GCs-stimulated BMECs. CHRDL2 overexpression could improve GCs-caused BMEC apoptosis and dysfunctions, possibly via the PI3K/Akt pathway.
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