Glioblastoma (GBM) is the most common malignant tumor of the central nervous system (CNS). It is a leading cause of death among patients with intracranial malignant tumors. GBM exhibits intra- and inter-tumor heterogeneity, leading to drug resistance and eventual tumor recurrence. Conventional treatments for GBM include maximum surgical resection of glioma tissue, temozolomide administration, and radiotherapy, but these methods do not effectively halt cancer progression. Therefore, development of novel methods for the treatment of GBM and identification of new therapeutic targets are urgently required. In recent years, studies have shown that drugs related to mitophagy and mitochondrial apoptosis pathways can promote the death of glioblastoma cells by inducing mitochondrial damage, impairing adenosine triphosphate (ATP) synthesis, and depleting large amounts of ATP. Some studies have also shown that modern nano-drug delivery technology targeting mitochondria can achieve better drug release and deeper tissue penetration, suggesting that mitochondria could be a new target for intervention and therapy. The combination of drugs targeting mitochondrial apoptosis and autophagy pathways with nanotechnology is a promising novel approach for treating GBM.This article reviews the current status of drug therapy for GBM, drugs targeting mitophagy and mitochondrial apoptosis pathways, the potential of mitochondria as a new target for GBM treatment, the latest developments pertaining to GBM treatment, and promising directions for future research.

Iron overload-associated osteoporosis presents a significant challenge to bone health. This study examines the effects of arecoline (ACL), an alkaloid found in areca nut, on bone metabolism under iron overload conditions induced by ferric ammonium citrate (FAC) treatment. The results indicate that ACL mitigates the FAC-induced inhibition of osteogenesis in zebrafish larvae, as demonstrated by increased skeletal mineralization and upregulation of osteogenic genes. ACL attenuates FAC-mediated suppression of osteoblast differentiation and mineralization in MC3T3-E1 cells. RNA sequencing analysis suggests that the protective effects of ACL are related to the regulation of ferroptosis. We demonstrate that ACL inhibits ferroptosis, including oxidative stress, lipid peroxidation, mitochondrial damage, and cell death under FAC exposure. In this study, we have identified heme oxygenase-1 (HO-1) as a critical mediator of ACL inhibiting ferroptosis and promoting osteogenesis, which was validated by HO-1 knockdown and knockout experiments. The study links ACL to HO-1 activation and ferroptosis regulation in the context of bone metabolism. These findings provide new insights into the mechanisms underlying the modulation of osteogenesis by ACL. Targeting the HO-1/ferroptosis axis is a promising therapeutic approach for treating iron overload-induced bone diseases.