坏死性下垂
自噬
骨髓
程序性细胞死亡
造血
活性氧
细胞
线粒体
干细胞
细胞生物学
癌症研究
生物
细胞凋亡
生物化学
免疫学
作者
Wanat Wudhikulprapan,Siriporn C. Chattipakorn,Nipon Chattipakorn,Sirinart Kumfu
标识
DOI:10.1016/j.abb.2024.109954
摘要
Iron overload has detrimental effects on bone marrow mesenchymal stem cells (BMMSCs), cells crucial for bone marrow homeostasis and hematopoiesis support. Excessive iron accumulation leads to the production of reactive oxygen species (ROS), resulting in cell death, cell cycle arrest, and disruption of vital cellular pathways. Although apoptosis has been extensively studied, other programmed cell death mechanisms including autophagy, necroptosis, and ferroptosis also play significant roles in iron overload-induced bone marrow cell death. Studies have highlighted the involvement of ROS production, DNA damage, MAPK pathways, and mitochondrial dysfunction in apoptosis. In addition, autophagy and ferroptosis are activated, as shown by the degradation of cellular components and lipid peroxidation, respectively. However, several compounds and antioxidants show promise in mitigating iron overload-induced cell death by modulating ROS levels, MAPK pathways, and mitochondrial integrity. Despite early indications, more comprehensive research and clinical studies are needed to better understand the interplay between these programmed cell death mechanisms and enable development of effective therapeutic strategies. This review article emphasizes the importance of studying multiple cell death pathways simultaneously and investigating potential rescuers to combat iron overload-induced bone marrow cell death.
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