Inflammation and oxidative stress as common mechanisms of pulmonary, autonomic, and musculoskeletal dysfunction after spinal cord injury

One of the etiopathogenic factors frequently associated with generalized organ damage after spinal cord injury corresponds to the imbalance of the redox state and inflammation, particularly of the respiratory, autonomic, and musculoskeletal systems. Our goal in this review was to gain a better under...

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Autores: Rosales-Antequera, Cristián, Viscor Carrasco, Ginés, Araneda, Oscar F.
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2022
País:España
Institución:Universidad de Barcelona
Repositorio:Dipòsit Digital de la UB
OAI Identifier:oai:diposit.ub.edu:2445/184837
Acceso en línea:https://hdl.handle.net/2445/184837
Access Level:acceso abierto
Palabra clave:Lesions medul·lars
Inflamació
Estrès oxidatiu
Spinal cord injuries
Inflammation
Oxidative stress
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spelling Inflammation and oxidative stress as common mechanisms of pulmonary, autonomic, and musculoskeletal dysfunction after spinal cord injuryRosales-Antequera, CristiánViscor Carrasco, GinésAraneda, Oscar F.Lesions medul·larsInflamacióEstrès oxidatiuSpinal cord injuriesInflammationOxidative stressOne of the etiopathogenic factors frequently associated with generalized organ damage after spinal cord injury corresponds to the imbalance of the redox state and inflammation, particularly of the respiratory, autonomic, and musculoskeletal systems. Our goal in this review was to gain a better understanding of this phenomenon by reviewing both animal and human studies. At the respiratory level, the presence of tissue damage is notable in situations that require increased ventilation due to lower thoracic distensibility and alveolar inflammation caused by higher levels of leptin as a result of increased fatty tissue. Increased airway reactivity, due to loss of sympathetic innervation, and levels of nitric oxide in exhaled air that are similar to those seen in asthmatic patients have also been reported. In addition, the loss of autonomic control efficiency leads to an uncontrolled release of catecholamines and glucocorticoids that induce immunosuppression, as well as a predisposition to autoimmune reactions. Simultaneously, blood pressure regulation is altered with vascular damage and atherogenesis associated with oxidative damage. At the muscular level, chronically elevated levels of prooxidants and lipoperoxidation associated with myofibrillar atrophy are described, with no reduction or reversibility of this process through antioxidant supplementationMDPI2022info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://hdl.handle.net/2445/184837Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)reponame:Dipòsit Digital de la UBinstname:Universidad de BarcelonaInglésReproducció del document publicat a: https://doi.org/10.3390/biology11040550Biology, 2022, vol. 11, num. 4, p. 550https://doi.org/10.3390/biology11040550cc-by (c) Rosales-Antequera, Cristián et al., 2022https://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:diposit.ub.edu:2445/1848372026-05-27T06:46:51Z
dc.title.none.fl_str_mv Inflammation and oxidative stress as common mechanisms of pulmonary, autonomic, and musculoskeletal dysfunction after spinal cord injury
title Inflammation and oxidative stress as common mechanisms of pulmonary, autonomic, and musculoskeletal dysfunction after spinal cord injury
spellingShingle Inflammation and oxidative stress as common mechanisms of pulmonary, autonomic, and musculoskeletal dysfunction after spinal cord injury
Rosales-Antequera, Cristián
Lesions medul·lars
Inflamació
Estrès oxidatiu
Spinal cord injuries
Inflammation
Oxidative stress
title_short Inflammation and oxidative stress as common mechanisms of pulmonary, autonomic, and musculoskeletal dysfunction after spinal cord injury
title_full Inflammation and oxidative stress as common mechanisms of pulmonary, autonomic, and musculoskeletal dysfunction after spinal cord injury
title_fullStr Inflammation and oxidative stress as common mechanisms of pulmonary, autonomic, and musculoskeletal dysfunction after spinal cord injury
title_full_unstemmed Inflammation and oxidative stress as common mechanisms of pulmonary, autonomic, and musculoskeletal dysfunction after spinal cord injury
title_sort Inflammation and oxidative stress as common mechanisms of pulmonary, autonomic, and musculoskeletal dysfunction after spinal cord injury
dc.creator.none.fl_str_mv Rosales-Antequera, Cristián
Viscor Carrasco, Ginés
Araneda, Oscar F.
author Rosales-Antequera, Cristián
author_facet Rosales-Antequera, Cristián
Viscor Carrasco, Ginés
Araneda, Oscar F.
author_role author
author2 Viscor Carrasco, Ginés
Araneda, Oscar F.
author2_role author
author
dc.subject.none.fl_str_mv Lesions medul·lars
Inflamació
Estrès oxidatiu
Spinal cord injuries
Inflammation
Oxidative stress
topic Lesions medul·lars
Inflamació
Estrès oxidatiu
Spinal cord injuries
Inflammation
Oxidative stress
description One of the etiopathogenic factors frequently associated with generalized organ damage after spinal cord injury corresponds to the imbalance of the redox state and inflammation, particularly of the respiratory, autonomic, and musculoskeletal systems. Our goal in this review was to gain a better understanding of this phenomenon by reviewing both animal and human studies. At the respiratory level, the presence of tissue damage is notable in situations that require increased ventilation due to lower thoracic distensibility and alveolar inflammation caused by higher levels of leptin as a result of increased fatty tissue. Increased airway reactivity, due to loss of sympathetic innervation, and levels of nitric oxide in exhaled air that are similar to those seen in asthmatic patients have also been reported. In addition, the loss of autonomic control efficiency leads to an uncontrolled release of catecholamines and glucocorticoids that induce immunosuppression, as well as a predisposition to autoimmune reactions. Simultaneously, blood pressure regulation is altered with vascular damage and atherogenesis associated with oxidative damage. At the muscular level, chronically elevated levels of prooxidants and lipoperoxidation associated with myofibrillar atrophy are described, with no reduction or reversibility of this process through antioxidant supplementation
publishDate 2022
dc.date.none.fl_str_mv 2022
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/184837
url https://hdl.handle.net/2445/184837
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Reproducció del document publicat a: https://doi.org/10.3390/biology11040550
Biology, 2022, vol. 11, num. 4, p. 550
https://doi.org/10.3390/biology11040550
dc.rights.none.fl_str_mv cc-by (c) Rosales-Antequera, Cristián et al., 2022
https://creativecommons.org/licenses/by/4.0/
info:eu-repo/semantics/openAccess
rights_invalid_str_mv cc-by (c) Rosales-Antequera, Cristián et al., 2022
https://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv MDPI
publisher.none.fl_str_mv MDPI
dc.source.none.fl_str_mv Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)
reponame:Dipòsit Digital de la UB
instname:Universidad de Barcelona
instname_str Universidad de Barcelona
reponame_str Dipòsit Digital de la UB
collection Dipòsit Digital de la UB
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15.300719

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