GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE301nnn/GSE301693/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE301693GEOGSEfalseAloe emodin alleviates ferroptosis mediated inhibition of cisplatin-induced osteogenic differentiation of BMSCS through Hippo-YAP1 signaling pathwayCisplatin (CDDP) chemotherapy induces bone loss partly by triggering ferroptosis and inhibiting osteogenic differentiation of bone marrow stromal cells (BMSCs). This study demonstrates that aloe-emodin (AE) rescues CDDP-impaired osteogenic differentiation in ST2 BMSCs by suppressing ferroptosis (reducing lipid peroxidation and iron accumulation), while concurrently enhancing death in 143B osteosarcoma cells. Mechanistically, AE activated the Hippo-YAP1 signaling pathway, increasing YAP1 protein levels and nuclear translocation. Bioinformatics and functional validation (YAP1 inhibitor Verteporfin and overexpression) confirmed that AE's anti-ferroptotic and pro-osteogenic effects critically depend on Hippo-YAP1 activation. Verteporfin abolished AE's protection, directly linking YAP1 to the reversal of CDDP-induced damage. This dual action of AE—bone protection via Hippo-YAP1-mediated ferroptosis inhibition in BMSCs and tumor suppression in osteosarcoma—highlights its therapeutic potential against chemotherapy-induced bone loss, revealing a novel strategy targeting the Hippo-YAP1-ferroptosis axis.2026/09/01GSE301693GSM9087469GSM9087471GSM9087470GSM9087464GSM9087472GSM9087468GSM9087467GSM9087466GSM908746517021301693Mus musculus