Protective Effects of Zinc on Spinal Cord Injury

Wen, Shan; Li, Yuanlong; Shen, Xiaolei; Wang, Zhe; Zhang, Kaihua; Zhang, Jiawei; Mei, Xifan

doi:10.1007/s12031-021-01859-x

Cited by 14 publications

(7 citation statements)

References 54 publications

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“…Interestingly, excess zinc is crucial in activating toxic autophagy induced by tamoxifen and H 2 O 2 [ 205 , 213 , 245 , 246 ]. After spinal cord injury, the serum zinc concentration decreases, the spinal cord zinc concentration increases at the injured site, and the zinc level in infiltrated monocytes increases significantly, which is equivalent to the injured spinal cord, and then zinc infiltrates the lesion area with monocytes [ 247 ]. Due to zinc chelation in senile plaques, the local zinc ion dynamics near amyloid aggregates in AD are unbalanced [ 74 ].…”

Section: Zinc and Autophagymentioning

confidence: 99%

Zinc in Cognitive Impairment and Aging

et al. 2022

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Zinc, an essential micronutrient for life, was first discovered in 1869 and later found to be indispensable for the normal development of plants and for the normal growth of rats and birds. Zinc plays an important role in many physiological and pathological processes in normal mammalian brain development, especially in the development of the central nervous system. Zinc deficiency can lead to neurodegenerative diseases, mental abnormalities, sleep disorders, tumors, vascular diseases, and other pathological conditions, which can cause cognitive impairment and premature aging. This study aimed to review the important effects of zinc and zinc-associated proteins in cognitive impairment and aging, to reveal its molecular mechanism, and to highlight potential interventions for zinc-associated aging and cognitive impairments.

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Section: Zinc and Autophagymentioning

confidence: 99%

Zinc in Cognitive Impairment and Aging

et al. 2022

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“…However, if administered at high concentrations, zinc can impair neurons through excitotoxicity, inducing oxidative stress and impairing cellular energy production. Therefore, the appropriate concentration of zinc could be used in SCI, but this dose has yet to be further defined [ 161 ].…”

Section: Supplements and Probiotics As Therapeutic Strategies After S...mentioning

confidence: 99%

Use of Cells, Supplements, and Peptides as Therapeutic Strategies for Modulating Inflammation after Spinal Cord Injury: An Update

Garcia,

Buzoianu-Anguiano,

Silva-Garcia

et al. 2023

IJMS

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Spinal cord injury is a traumatic lesion that causes a catastrophic condition in patients, resulting in neuronal deficit and loss of motor and sensory function. That loss is caused by secondary injury events following mechanical damage, which results in cell death. One of the most important events is inflammation, which activates molecules like proinflammatory cytokines (IL-1β, IFN-γ, and TNF-α) that provoke a toxic environment, inhibiting axonal growth and exacerbating CNS damage. As there is no effective treatment, one of the developed therapies is neuroprotection of the tissue to preserve healthy tissue. Among the strategies that have been developed are the use of cell therapy, the use of peptides, and molecules or supplements that have been shown to favor an anti-inflammatory environment that helps to preserve tissue and cells at the site of injury, thus favoring axonal growth and improved locomotor function. In this review, we will explain some of these strategies used in different animal models of spinal cord injury, their activity as modulators of the immune system, and the benefits they have shown.

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“…By the way, HOs are mediators of oxidative injury and affect cellular redox homeostasis, which indicates that HOs are related to the occurrence of ferroptosis. Previous studies have reported that DNA damage exists, irrespective of the acute or chronic phases of nerve injury, thereby causing a series of adverse reactions, such as intracellular protein oxidation and inactivation [94,95]. Apart from DNA and protein damage, lipid metabolism also plays a key role in the neuroimmune communication during nerve injury-induced NP.…”

Section: Ferroptosis In the Schwann Cells After Peripheral Nervementioning

confidence: 99%

Iron Metabolism and Ferroptosis in Peripheral Nerve Injury

Huang

Bian

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Peripheral nerve injury (PNI) is a major clinical problem that may lead to different levels of sensory and motor dysfunction including paralysis. Due to the high disability rate and unsatisfactory prognosis, the exploration and revealment of the mechanisms involved in the PNI are urgently required. Ferroptosis, a recently identified novel form of cell death, is an iron-dependent process. It is a unique modality of cell death, closely associated with iron concentrations, generation of reactive oxygen species, and accumulation of the lipid reactive oxygen species. These processes are regulated by multiple cellular metabolic pathways, including iron overloading, lipid peroxidation, and the glutathione/glutathione peroxidase 4 pathway. Furthermore, ferroptosis is accompanied by morphological changes in the mitochondria, such as increased membrane density and shrunken mitochondria; this association between ferroptosis and mitochondrial damage has been detected in various diseases, including spinal cord injury and PNI. The inhibition of ferroptosis can promote the repair of damaged peripheral nerves, reduce mitochondrial damage, and promote the recovery of neurological function. In this review, we intend to discuss the detailed mechanisms of ferroptosis and summarize the current researches on ferroptosis with respect to nerve injury. This review also aims at providing new insights on targeting ferroptosis for PNI treatment.

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Protective Effects of Zinc on Spinal Cord Injury

Cited by 14 publications

References 54 publications

Zinc in Cognitive Impairment and Aging

Zinc in Cognitive Impairment and Aging

Use of Cells, Supplements, and Peptides as Therapeutic Strategies for Modulating Inflammation after Spinal Cord Injury: An Update

Iron Metabolism and Ferroptosis in Peripheral Nerve Injury

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