The Role of Magnesium in the Secondary Phase After Traumatic Spinal Cord Injury. A Prospective Clinical Observer Study

Sperl, André; Heller, Raban Arved; Biglari, Bahram; Haubruck, Patrick; Seelig, Julian; Schomburg, Lutz; Bock, Tobias; Moghaddam, Arash

doi:10.3390/antiox8110509

Cited by 15 publications

(12 citation statements)

References 52 publications

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“…Previous studies indicated that peripheral trace element dynamics and concentration changes in the trace element biomarkers are associated with the clinical outcome after TSCI ( Heller et al, 2019 , 2020 ; Sperl et al, 2019 ; Seelig et al, 2020 ). It was thus hypothesized that there might be a close correlation between serum Se, SELENOP and SELENBP1 concentrations.…”

Section: Discussionmentioning

confidence: 99%

Selenium-Binding Protein 1 (SELENBP1) as Biomarker for Adverse Clinical Outcome After Traumatic Spinal Cord Injury

et al. 2021

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Graphical AbstractThe pathophysiology of traumatic spinal cord injury (TSCI) can be divided into two major phases. (A) The mechanical trauma is followed within minutes by a secondary phase consisting of local complex and intertwined acute responses, intercellular signaling and cell activity regulating pathways. Inflammatory processes, oxidative stress and hypoxia, leading to cell damage and death, and specific cell contents are released into the circulation (B). The motor and sensory deficits upon TSCI are assessed by using the American Spinal Injury Association (ASIA) impairment scale (AIS), ranging from AIS A as a complete absence of any motor and sensory functions under the lesion site, to AIS E with complete preservation of motor and sensory functions. (C) The concentrations of serum SELENBP1 were elevated in patients classified as AIS A as compared to less severely affected patients classified as AIS B, C or D. A cut-off was deduced [(SELENBP1) > 30.2 μg/L], reliably predicting whether a patient belongs to the group showing neurological recovery (G1) or not (G0) within 3 months after the trauma. The figure was created by using https://biorender.com.

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Section: Discussionmentioning

confidence: 99%

Selenium-Binding Protein 1 (SELENBP1) as Biomarker for Adverse Clinical Outcome After Traumatic Spinal Cord Injury

et al. 2021

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“…They can trigger different regulatory functions through specific ion channels and enzymes. Recent studies have revealed that membrane significant fluxes of Mg 2+ can affect the cell’s metabolic cycles and function [ 83 ]. In the central nervous system, Mg 2+ is known to maintain calcium homeostasis.…”

Section: Magnesium and Cellular Biology Of Scimentioning

confidence: 99%

Main Cations and Cellular Biology of Traumatic Spinal Cord Injury

Munteanu

Rotariu

Turnea

et al. 2022

Cells

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Traumatic spinal cord injury is a life-changing condition with a significant socio-economic impact on patients, their relatives, their caregivers, and even the community. Despite considerable medical advances, there is still a lack of options for the effective treatment of these patients. The major complexity and significant disabling potential of the pathophysiology that spinal cord trauma triggers are the main factors that have led to incremental scientific research on this topic, including trying to describe the molecular and cellular mechanisms that regulate spinal cord repair and regeneration. Scientists have identified various practical approaches to promote cell growth and survival, remyelination, and neuroplasticity in this part of the central nervous system. This review focuses on specific detailed aspects of the involvement of cations in the cell biology of such pathology and on the possibility of repairing damaged spinal cord tissue. In this context, the cellular biology of sodium, potassium, lithium, calcium, and magnesium is essential for understanding the related pathophysiology and also the possibilities to counteract the harmful effects of traumatic events. Lithium, sodium, potassium—monovalent cations—and calcium and magnesium—bivalent cations—can influence many protein–protein interactions, gene transcription, ion channel functions, cellular energy processes—phosphorylation, oxidation—inflammation, etc. For data systematization and synthesis, we used the Preferred Reporting Items for Systematic Reviews and Meta-Analyzes (PRISMA) methodology, trying to make, as far as possible, some order in seeing the “big forest” instead of “trees”. Although we would have expected a large number of articles to address the topic, we were still surprised to find only 51 unique articles after removing duplicates from the 207 articles initially identified. Our article integrates data on many biochemical processes influenced by cations at the molecular level to understand the real possibilities of therapeutic intervention—which must maintain a very narrow balance in cell ion concentrations. Multimolecular, multi-cellular: neuronal cells, glial cells, non-neuronal cells, but also multi-ionic interactions play an important role in the balance between neuro-degenerative pathophysiological processes and the development of effective neuroprotective strategies. This article emphasizes the need for studying cation dynamics as an important future direction.

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“…level to 40-60% with a 10-15% decrease in total Mg 2? level; which may affect the entry of glutamate and calcium into the presynaptic neuron (Sperl et al 2019;Cook et al 2011). This results in neurodegeneration and cell death as secondary to brain injury (Institute of Medicine (US) Committee on Nutrition 2011).…”

Section: Magnesium and Neurological Diseasesmentioning

confidence: 99%

‘Magnesium’-the master cation-as a drug—possibilities and evidences

Mathew

Panonnummal

2021

Biometals

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Magnesium (Mg 2? ) is the 2nd most abundant intracellular cation, which participates in various enzymatic reactions; there by regulating vital biological functions. Magnesium (Mg 2? ) can regulate several cations, including sodium, potassium, and calcium; it consequently maintains physiological functions like impulse conduction, blood pressure, heart rhythm, and muscle contraction. But, it doesn't get much attention in account with its functions, making it a ''Forgotten cation''. Like other cations, maintenance of the normal physiological level of Mg 2? is important. Its deficiency is associated with various diseases, which point out to the importance of Mg 2? as a drug. The roles of Mg 2? such as natural calcium antagonist, glutamate NMDA receptor blocker, vasodilator, antioxidant and anti-inflammatory agent are responsible for its therapeutic benefits. Various salts of Mg 2? are currently in clinical use, but their application is limited. This review collates all the possible mechanisms behind the behavior of magnesium as a drug at different disease conditions with clinical shreds of evidence. Keywords Magnesium Á Calcium antagonist Á Hypomagnesemia Á NMDA blocker Á Forgotten cation Á Vasodilator Abbreviations ACE Angiotensin converting enzyme AD Alzheimer's disease (AD) ALP Alkaline phosphatase ALT Aminotransferase AMPA a-Amino-3-hydroxy-5-methyl-4isoxazolepropionic acid APP Amyloid precursor protein AST Aspartate aminotransferase ATP Adenosine triphosphate BBB Blood brain barrier BMD Bone mineral density BMP2 Bone morphogenetic protein 2 BP Blood pressure cAMP Cyclic Adenosine mono phosphate CAD Coronary arytery diseases CFTR Cystic fibrosis transmembrane conductance regulator CGRP Calcitonin gene related peptide CHF Congestive heart Failure Claudin CLDN CNS Central nervous system CSD Cortical spreading depression CSF Cerebrospinal fluid CTF b C terminal fragment b CVD Cardiovascular diseases

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The Role of Magnesium in the Secondary Phase After Traumatic Spinal Cord Injury. A Prospective Clinical Observer Study

Cited by 15 publications

References 52 publications

Selenium-Binding Protein 1 (SELENBP1) as Biomarker for Adverse Clinical Outcome After Traumatic Spinal Cord Injury

Selenium-Binding Protein 1 (SELENBP1) as Biomarker for Adverse Clinical Outcome After Traumatic Spinal Cord Injury

Main Cations and Cellular Biology of Traumatic Spinal Cord Injury

‘Magnesium’-the master cation-as a drug—possibilities and evidences

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