P=N/A, N=24, Not yet recruiting, Dermatology Hospital of Southern Medical University; Dermatology Hospital of Southern Medical University

P=N/A, N=22, Not yet recruiting, Shanghai Pulmonary Hospital; Shanghai Pulmonary Hospital

P=N/A, N=210, Not yet recruiting, Affiliated Mental Health Center & Hangzhou Seventh People's Hospital, Zhejiang University School of Medicine; Affiliated Mental Health Center &amp

P=N/A, N=90, Recruiting, Shanghai University of Traditional Chinese Medicine; Shanghai University of Traditional Chinese Medicine

P=N/A, N=20, Completed, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Provincial People's Hospital.; Jiangsu Provincial People's Hospital

P4, N=250, Recruiting, Shenzhen Second People's Hospital; Shenzhen Second People's Hospital

P4, N=50, Not yet recruiting, Dongzhimen Hospital, Beijing University of Chinese Medicine; Dongzhimen Hospital, Beijing University of Chinese Medicine

P2, N=48, Recruiting, Shanghai Ninth People's Hospital， Shanghai JiaoTong University School of Medicine; Shanghai Ninth People's Hospital， Shanghai JiaoTong University

qPCR and flow cytometry analyses further confirmed that simvastatin exerted its therapeutic effects by suppressing the calcium signaling pathway and downregulating the expression of nuclear factor of activated T cells 3 (NFATC3). Collectively, our study demonstrates that simvastatin alleviates CD4+ T cell inflammatory responses in AIH through calcium-dependent signaling pathway.

The combination of rosuvastatin and bortezomib exerts a synergistic effect by inhibiting CCL3, thereby rebalancing bone remodeling and promoting osteogenesis. This strategy represents a promising novel therapeutic approach for mitigating MBD.

The combination of rosuvastatin and meloxicam at specific concentrations increased the radiation sensitivity of MCF-7, T-47D, and MDA-MB-231 cells. Combined pretreatment with rosuvastatin 10 μM and meloxicam 50 μM notably enhanced genotoxicity while reducing colony formation, catalase activity, and SOD activity compared to radiotherapy alone in MCF-7, T-47D, and MDA-MB-231 cell lines.

CAV1 gene silencing by siRNA validated its role in maintenance of stem-like phenotype and metabolic alterations of GBM spheroids. Collectively, this study demonstrated the regulatory role of Caveolin1 and cholesterol in maintaining stem-like characteristics of GBM spheroids and the importance of tumor models in better understanding of the molecular mechanism of GBM.Key words: Glioblastoma, cholesterol biosynthesis, stemness, Caveolin1, DNMT1, KDM5A, Gli1.