ArticleOxidative medicine and cellular longevity2022
Cyclic Polypeptide D7 Protects Bone Marrow Mesenchymal Cells and Promotes Chondrogenesis during Osteonecrosis of the Femoral Head via Growth Differentiation Factor 15-Mediated Redox Signaling.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 25 citations in OpenAlex.
- Harmine ameliorates steroid-induced osteonecrosis of the femoral head by modulating metabolism and ferroptosis via HIF1-α.Fundamental research · 2026Article
- Advances in the mechanism for steroid-induced osteonecrosis of the femoral head.Bone research · 2026Review
- Endoplasmic reticulum stress in steroid-induced osteonecrosis: translational bottlenecks and targeted therapeutic strategies.Frontiers in pharmacology · 2026Review
- Total hip arthroplasty and perioperative management of a patient with hip osteonecrosis secondary to hypopituitarism due to Sheehan syndrome: a case report and literature review.Frontiers in surgery · 2026Article
- YTHDF3-associated m6A regulation and cuproptosis-related gene expression in steroid-induced osteonecrosis of the femoral head.Journal of molecular histology · 2025Article
- Recent advances in osteonecrosis of the femoral head: a focus on mesenchymal stem cells and adipocytes.Journal of translational medicine · 2025Review
- B-Lymphoid Tyrosine Kinase Crosslinks Redox and Apoptosis Signaling Networks to Promote the Survival of Transplanted Bone Marrow Mesenchymal Stem Cells.Research (Washington, D.C.) · 2025Article
- Senescence-associated secretory phenotype in lung cancer: remodeling the tumor microenvironment for metastasis and immune suppression.Frontiers in oncology · 2025Review
- Crebanine mitigates glucocorticoid-induced osteonecrosis of the femoral head by restoring bone remodelling homeostasis via attenuating oxidative stress.Journal of cellular and molecular medicine · 2024Article
- Inhibition of insulin degrading enzyme suppresses osteoclast hyperactivity via enhancing Nrf2-dependent antioxidant response in glucocorticoid-induced osteonecrosis of the femoral head.Molecular medicine (Cambridge, Mass.) · 2024Article
- Inhibition of Protein Disulfide Isomerase Attenuates Osteoclast Differentiation and Function via the Readjustment of Cellular Redox State in Postmenopausal Osteoporosis.Inflammation · 2024Article
- Cortistatin prevents glucocorticoid-associated osteonecrosis of the femoral head via the GHSR1a/Akt pathway.Communications biology · 2024Article
- Glucocorticoid-induced activation of NOX/ROS/NF-κB signaling in MSCs contributes to the development of GONFH.Apoptosis : an international journal on programmed cell death · 2023Article
- Exogenous melatonin ameliorates steroid-induced osteonecrosis of the femoral head by modulating ferroptosis through GDF15-mediated signaling.Stem cell research & therapy · 2023Article
- Identification and Validation of Potential Ferroptosis-Related Genes in Glucocorticoid-Induced Osteonecrosis of the Femoral Head.Medicina (Kaunas, Lithuania) · 2023Article
- Macrophages in aseptic loosening: Characteristics, functions, and mechanisms.Frontiers in immunology · 2023Review
- Bilibili and TikTok as sources of medical information on osteonecrosis of the femoral head: A cross-platform content analysis.Digital healthArticle
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
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Abstract
Osteonecrosis of the femoral head (ONFH) is a debilitating disease that is closely associated with the clinical application of high-dose glucocorticoids. Elevated oxidative stress contributes to the pathophysiological changes observed in ONFH. The lack of effective treatments besides surgical intervention highlights the importance of finding novel therapeutics. Our previous studies demonstrated that D7, a cyclic polypeptide, enhances the adhesion, expansion, and proliferation of bone marrow mesenchymal stem cells (BMSCs). Therefore, in this study, we investigated the therapeutic effects of D7 against ONFH in BMSCs and evaluated the underlying mechanisms. First, we screened for ONFH risk factors. Then, we applied D7 treatment to steroid-induced ONFH (SONFH) in an in vitro model produced by dexamethasone (DEX) to further elucidate the underlying mechanisms. We found negative correlations among oxidative stress marker expression, growth differentiation factor 15 (GDF15) levels, and ONFH. Furthermore, we demonstrated that DEX inhibited the proliferation and induced apoptosis of BMSCs by suppressing GDF15/AKT/mammalian target of rapamycin (mTOR) signaling. D7 alleviated DEX-induced BMSCs injury and restored the chondrogenic function of BMSCs by activating GDF15/AKT/mTOR signaling. In addition, DEX-induced excessive reactive oxygen species (ROS) generation was an upstream trigger of GDF15-mediated signaling, and D7 ameliorated this DEX-induced redox imbalance by restoring the expression of antioxidants, including superoxide dismutase (SOD) 1, SOD2, and catalase, via regulation of GDF15 expression. In conclusion, our findings revealed the potential therapeutic effects of D7 in SONFH and showed that this protective function may be mediated via inhibition of DEX-induced ROS and activation of GDF15/AKT/mTOR signaling, thereby providing insights into the potential applications of D7 in SONFH treatment.
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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.