Mesenchymal stem cells, extracellular vesicles, and transcranial magnetic stimulation for ferroptosis after spinal cord injury

Abstract

Spinal cord injury is characterized by different aetiologies, complex pathogenesis, and diverse pathological changes. Current treatments are not ideal, and prognosis is generally poor. After spinal cord injury, neurons die due to various forms of cell death. Among them, ferroptosis causes dysfunction after spinal cord injury, and no existing traditional treatments have been indicated to block its occurrence. Meanwhile, emerging therapies using mesenchymal stem cells, extracellular vesicles, and transcranial magnetic stimulation therapy are promising for reversing spinal cord neuronal ferroptosis after spinal cord injury. However, no definitive studies have demonstrated the effectiveness of these approaches. This review summarizes the existing research on the mechanisms of ferroptosis; ferroptosis after spinal cord injury; treatment of spinal cord injury with mesenchymal stem cells, extracellular vesicles, and transcranial magnetic stimulation; and treatment of ferroptosis using mesenchymal stem cells, extracellular vesicles, and transcranial magnetic stimulation. Inhibiting ferroptosis can promote the reversal of neurological dysfunction after spinal cord injury. In addition, mesenchymal stem cells, extracellular vesicles, and transcranial magnetic stimulation can reverse adverse outcomes of spinal cord injury and regulate ferroptosis-related factors. Thus, it can be inferred that mesenchymal stem cells, extracellular vesicles, and transcranial magnetic stimulation have the potential to inhibit ferroptosis after spinal cord injury. This review serves as a reference for future research to confirm these conclusions.

Ferroptosis: a new regulatory mechanism in neuropathic pain

“…And in a related study, it was found that treatment with ferrostatin-1 significantly inhibited the onset of oxidative stress in brain tissue, improved the structure of brain tissue after hemorrhage, protected neurons, and promoted neurological function in recovery of rats. Another specific inhibitor, liproxstatin-1 (Lip-1), also significantly inhibited the elevated levels of ROS induced by mitochondrial lipid peroxidation and restored GPX4 expression levels, which in turn effectively reduced chronic compression injury of the rat ( Song et al, 2023 ). A recent study showed that CCI-induced mechanical and thermal nociceptive abnormalities in rats were significantly alleviated by intraperitoneal injection of Lip-1, while a decrease in iron content and a reduction in lipid peroxidation responses in spinal cord tissue were observed, along with a return to normal GPX4 expression levels.…”