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Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

Anjum, Anam, Yazid, Muhammad Da’in, Fauzi Daud, Muhammad, Idris, Jalilah, Ng, Angela Min Hwei, Selvi Naicker, Amaramalar, Ismail, Ohnmar Htwe@ Rashidah, Athi Kumar, Ramesh Kumar, Lokanathan, Yogeswaran·2020·International Journal of Molecular Sciences
DOI 10.3390/ijms21207533PMC PMC7589539
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Abstract

Spinal cord injury (SCI) is a destructive neurological and pathological state that causes major motor, sensory and autonomic dysfunctions. Its pathophysiology comprises acute and chronic phases and incorporates a cascade of destructive events such as ischemia, oxidative stress, inflammatory events, apoptotic pathways and locomotor dysfunctions. Many therapeutic strategies have been proposed to overcome neurodegenerative events and reduce secondary neuronal damage. Efforts have also been devoted in developing neuroprotective and neuro-regenerative therapies that promote neuronal recovery and outcome. Although varying degrees of success have been achieved, curative accomplishment is still elusive probably due to the complex healing and protective mechanisms involved. Thus, current understanding in this area must be assessed to formulate appropriate treatment modalities to improve SCI recovery. This review aims to promote the understanding of SCI pathophysiology, interrelated or interlinked multimolecular interactions and various methods of neuronal recovery i.e., neuroprotective, immunomodulatory and neuro-regenerative pathways and relevant approaches.

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Figure 1 Spinal cord injury (SCI) (a) phases of SCI, (b) sub-classification of secondary injury depending on duration of injury and (c) pathophysiological events according to SCI phases.
Figure 1 Spinal cord injury (SCI) (a) phases of SCI, (b) sub-classification of secondary injury depending on duration of injury and (c) pathophysiological events according to SCI phases.CC BY · PubMed Central
Figure 2 Pathophysiology, clinical manifestations, and phases of SCI.
Figure 2 Pathophysiology, clinical manifestations, and phases of SCI.CC BY · PubMed Central
Figure 3 Stages of axon degeneration, (A) acute injury responses, (B) acute axonal degeneration (AAD) and (C) Wallerian degeneration.
Figure 3 Stages of axon degeneration, (A) acute injury responses, (B) acute axonal degeneration (AAD) and (C) Wallerian degeneration.CC BY · PubMed Central
Figure 4 (A) Healthy spinal cord and (B) an injured spinal cord with three lesion compartments, showing inner non-viable small lesion compartment, compact astrocyte core, and perilesion perimeters with multicellular and multi-molecular components (astrocytes, neurons, macrophages, microglia, NG2-OPC, fibrocytes, oligodendrocytes, fibroblast, nerve cells and activated astrocytes) regulating gliosis (gliosis scar formation) post SCI.
Figure 4 (A) Healthy spinal cord and (B) an injured spinal cord with three lesion compartments, showing inner non-viable small lesion compartment, compact astrocyte core, and perilesion perimeters with multicellular and multi-molecular components (astrocytes, neurons, macrophages, microglia, NG2-OPC, fibrocytes, oligodendrocytes, fibroblast, nerve cells and activated astrocytes) regulating gliosis (gliosis scar formation) post SCI.CC BY · PubMed Central
Figure 5 Molecular interactions balancing inflammatory responses, debris clearance and phagocytosis regulators following SCI with left showing hydrophobic intercellular molecular interactions controlling harmful signal while right cycle reflect neuro-inflammatory molecular interaction controlling phagocytosis while center portion show multimolecular interactions to clear cellular phagocytic debris.
Figure 5 Molecular interactions balancing inflammatory responses, debris clearance and phagocytosis regulators following SCI with left showing hydrophobic intercellular molecular interactions controlling harmful signal while right cycle reflect neuro-inflammatory molecular interaction controlling phagocytosis while center portion show multimolecular interactions to clear cellular phagocytic debris.CC BY · PubMed Central
Figure 6 Neuroprotective pathways and different neuroprotective approaches with centre portion showing neuroprotective pathways (i) neurotransmitter agonist/antagonist, (ii) channel blockers, (iii) anti-oxidative pathways, (iv) apoptotic pathway (v) herbal and natural agents, (vi) cellular and genetic agents, while various agents acting on specific pathways are shown by pointed arrows.
Figure 6 Neuroprotective pathways and different neuroprotective approaches with centre portion showing neuroprotective pathways (i) neurotransmitter agonist/antagonist, (ii) channel blockers, (iii) anti-oxidative pathways, (iv) apoptotic pathway (v) herbal and natural agents, (vi) cellular and genetic agents, while various agents acting on specific pathways are shown by pointed arrows.CC BY · PubMed Central
Figure 7 Apoptotic pathway (i) intrinsic pathway and (ii) extrinsic pathway with anti-apoptotic inhibitors, i.e., calpain and caspase that act on specific target molecule and retard apoptosis.
Figure 7 Apoptotic pathway (i) intrinsic pathway and (ii) extrinsic pathway with anti-apoptotic inhibitors, i.e., calpain and caspase that act on specific target molecule and retard apoptosis.CC BY · PubMed Central
Figure 8 Immuno-modulatory (neuro-inflammatory) pathway following spinal cord injury and specific immuno-modulatory agents.
Figure 8 Immuno-modulatory (neuro-inflammatory) pathway following spinal cord injury and specific immuno-modulatory agents.CC BY · PubMed Central
Figure 9 Neuroregenerative pathway (RhoA/Rho and Rock pathway) and underlying neuroregenerative approaches (i) enhancement of remyelination and (ii) enhancement of neuronal and axonal regeneration strategies.
Figure 9 Neuroregenerative pathway (RhoA/Rho and Rock pathway) and underlying neuroregenerative approaches (i) enhancement of remyelination and (ii) enhancement of neuronal and axonal regeneration strategies.CC BY · PubMed Central

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Metadata

Authors
Anjum, A., Yazid, M. D., Fauzi Daud, M., Idris, J., Ng, A. M. H., Selvi Naicker, A., Ismail, O. H. R., Athi Kumar, R. K., & Lokanathan, Y.
Affiliations
  • Centre for Tissue Engineering and Regenerative Medicine, Faculty of Medicine, Universiti Kebangsaan Malaysia, Jalan Yaccob Latiff, Cheras, Kuala Lumpur 56000, Malaysia
  • Institute of Medical Science Technology, Universiti Kuala Lumpur Malaysia, Kajang 43000, Malaysia
  • Department of Orthopaedics & Traumatology, Faculty of Medicine, Universiti Kebangsaan Malaysia, Kuala Lumpur 56000, Malaysia
  • Department of Surgery, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latiff, Bandar Tun Razak, Kuala Lumpur 56000, Malaysia
ORCID
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2020-10-13
Volume
21
Issue
20
Pages
7533
ISSN
1422-0067
DOI
10.3390/ijms21207533
PMC
PMC7589539
Cited by
1,270
References
8
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
Universiti Kebangsaan Malaysia (FF-2019-542/1)

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