Alpha-tocopherol inhibits ferroptosis and promotes neural function recovery in rats with spinal cord injury via downregulating Alox15

Zhu, Rui; Kang, Yu; Li, Qiangwei; Peng, Kai; Shi, Xuanming; Yin, Zongsheng; Xuan, Yong

doi:10.1016/j.biopha.2024.116734

Cited by 5 publications

References 54 publications

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Analyzing the role of ferroptosis in ribosome‐related bone marrow failure disorders: From pathophysiology to potential pharmacological exploitation

Papadimitriou‐Tsantarliotou,

Avgeros,

Konstantinidou

et al. 2024

IUBMB Life

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Within the last decade, the scientific community has witnessed the importance of ferroptosis as a novel cascade of molecular events leading to cellular decisions of death distinct from apoptosis and other known forms of cell death. Notably, such non‐ apoptotic and iron‐dependent regulated cell death has been found to be intricately linked to several physiological processes as well as to the pathogenesis of various diseases. To this end, recent data support the notion that a potential molecular connection between ferroptosis and inherited bone marrow failure (IBMF) in individuals with ribosomopathies may exist. In this review, we suggest that in ribosome‐related IBMFs the identified mutations in ribosomal proteins lead to changes in the ribosome composition of the hematopoietic progenitors, changes that seem to affect ribosomal function, thus enhancing the expression of some mRNAs subgroups while reducing the expression of others. These events lead to an imbalance inside the cell as some molecular pathways are promoted while others are inhibited. This disturbance is accompanied by ROS production and lipid peroxidation, while an additional finding in most of them is iron accumulation. Once lipid peroxidation and iron accumulation are the two main characteristics of ferroptosis, it is possible that this mechanism plays a key role in the manifestation of IBMF in this type of disease. If this molecular mechanism is further confirmed, new pharmacological targets such as ferroptosis inhibitors that are already exploited for the treatment of other diseases, could be utilized to improve the treatment of ribosomopathies.

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Analyzing the role of ferroptosis in ribosome‐related bone marrow failure disorders: From pathophysiology to potential pharmacological exploitation

Papadimitriou‐Tsantarliotou,

Avgeros,

Konstantinidou

et al. 2024

IUBMB Life

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Ferroptosis in the neurovascular unit after spinal cord injury

Huang,

Bai

2024

Experimental Neurology

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Physiologic Regulation of Lipid Oxidation and Ferroptosis By Vitamin E, High-Density Lipoprotein, and Scavenger Receptor Class B Type 1

Rink,

Calvert,

Moxley

et al. 2024

Preprint

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Ferroptosis is a form of cell death caused by oxidative (-OOH) damage to phospholipids (PL) that comprise the cell membrane. Understanding mechanisms of ferroptosis is important because of the role it plays in human disease, including cancer and neurodegeneration. Previous work has focused on the intracellular antioxidant enzyme glutathione peroxidase 4 (GPx4), which detoxifies PL-peroxides (PL-OOH) and prevents ferroptosis. Studies also show that alpha-tocopherol (α-toc), the active form of Vitamin E, is an exogenous lipophilic antioxidant that inhibits ferroptosis in cancer cells in vitro and in neurons and hematopoietic stem cells in vivo. The mechanisms by which α-toc engages cells to manipulate PL redox balance and ferroptosis are unknown. Lipoproteins, like high- and low-density lipoproteins (HDL and LDL), carry α-toc in the circulation, which compelled our investigation of their role in α-toc delivery and ferroptosis. Using cancer and neuronal cell models, here we show that lipoproteins, particularly HDL, deliver α-toc by binding the cell membrane receptor scavenger receptor class B type 1 (SR-B1) to prevent ferroptosis. Additionally, we synthesized SR-B1 targeted HDL-like particles that contained α-toc to validate data obtained with native lipoproteins. We reveal here a tunable cellular redox axis whereby native and synthetic HDLs containing α-toc target SR-B1 to reduce PL-OOH and prevent ferroptosis.

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Alpha-tocopherol inhibits ferroptosis and promotes neural function recovery in rats with spinal cord injury via downregulating Alox15

Cited by 5 publications

References 54 publications

Analyzing the role of ferroptosis in ribosome‐related bone marrow failure disorders: From pathophysiology to potential pharmacological exploitation

Analyzing the role of ferroptosis in ribosome‐related bone marrow failure disorders: From pathophysiology to potential pharmacological exploitation

Ferroptosis in the neurovascular unit after spinal cord injury

Physiologic Regulation of Lipid Oxidation and Ferroptosis By Vitamin E, High-Density Lipoprotein, and Scavenger Receptor Class B Type 1

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