Author(s):
Breast cancer, a multifaceted and prevalent disease, remains a formidable challenge in oncology. Recent advances have highlighted the role of mitochondria-related signaling pathways in shaping breast cancer progression and response to treatment. Intriguingly, these pathways intersect with the regulation of ferroptosis, a unique form of cell death characterized by lipid peroxidation. This article reviews the intricate connections between mitochondria-related signaling and ferroptosis in breast cancer [1 , 2]. It explores the impact of mitochondrial metabolism, ROS production, apoptosis regulation, and quality control on ferroptotic susceptibility. The potential therapeutic implications of targeting these pathways to enhance ferroptosis in breast cancer are also discussed, offering insights into innovative treatment strategies and highlighting a promising avenue for improving patient outcomes [3].
