Neuroinflammation in Age-Related Neurodegenerative Diseases: Role of Mitochondrial Oxidative Stress
A shared hallmark of age-related neurodegenerative diseases is the chronic activation of innate immune cells, which actively contributes to the neurodegenerative process. In Alzheimer’s disease, this inflammatory milieu exacerbates both amyloid and tau pathology. A similar abnormal inflammatory resp...
| Autores: | , , , , , , , , , , , |
|---|---|
| Formato: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2024 |
| País: | España |
| Recursos: | Universidad de Sevilla (US) |
| Repositorio: | idUS. Depósito de Investigación de la Universidad de Sevilla |
| OAI Identifier: | oai:idus.us.es:11441/170534 |
| Acesso em linha: | https://hdl.handle.net/11441/170534 https://doi.org/10.3390/antiox13121440 |
| Access Level: | acceso abierto |
| Palavra-chave: | Cuproptosis Ferroptosis Inflammasomes Mitochondria Mitochondrial oxidative stress Necroptosis Neuroinflammation Pyroptosis |
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Neuroinflammation in Age-Related Neurodegenerative Diseases: Role of Mitochondrial Oxidative StressAbadin, X.Dios, Cristina deZubillaga, M.Ivars, E.Puigròs, M.Marí, M.Morales, A.Vizuete Chacón, María LuisaVitorica Ferrández, Francisco JavierTrullas, R.Colell, A.Roca Agujetas, VicenteCuproptosisFerroptosisInflammasomesMitochondriaMitochondrial oxidative stressNecroptosisNeuroinflammationPyroptosisA shared hallmark of age-related neurodegenerative diseases is the chronic activation of innate immune cells, which actively contributes to the neurodegenerative process. In Alzheimer’s disease, this inflammatory milieu exacerbates both amyloid and tau pathology. A similar abnormal inflammatory response has been reported in Parkinson’s disease, with elevated levels of cytokines and other inflammatory intermediates derived from activated glial cells, which promote the progressive loss of nigral dopaminergic neurons. Understanding the causes that support this aberrant inflammatory response has become a topic of growing interest and research in neurodegeneration, with high translational potential. It has been postulated that the phenotypic shift of immune cells towards a proinflammatory state combined with the presence of immunogenic cell death fuels a vicious cycle in which mitochondrial dysfunction plays a central role. Mitochondria and mitochondria-generated reactive oxygen species are downstream effectors of different inflammatory signaling pathways, including inflammasomes. Dysfunctional mitochondria are also recognized as important producers of damage-associated molecular patterns, which can amplify the immune response. Here, we review the major findings highlighting the role of mitochondria as a checkpoint of neuroinflammation and immunogenic cell deaths in neurodegenerative diseases. The knowledge of these processes may help to find new druggable targets to modulate the inflammatory response.Ministerio de Ciencia e Innovación PID2022-143279OB-100, PID2021-123564OB-100, PDC2023-145806-100, PID2020-115091RB-I00, RED2022-134786-TInstituto de Salud Carlos III PMP22/00100, PI22/00475Generalitat de Catalunya 2021-SGR00490Junta de Andalucía US-1262734, P20-00843Agencia Estatal de Investigación JDC2022-048952-IEuropean Union 2022 INV-1 00065Multidisciplinary Digital Publishing Institute (MDPI)Bioquímica y Biología MolecularMinisterio de Ciencia e Innovación (MICIN). EspañaInstituto de Salud Carlos IIIGeneralitat de CatalunyaJunta de AndalucíaAgencia Estatal de Investigación. EspañaEuropean Union (UE)2024info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfapplication/pdfhttps://hdl.handle.net/11441/170534https://doi.org/10.3390/antiox13121440reponame:idUS. Depósito de Investigación de la Universidad de Sevillainstname:Universidad de Sevilla (US)InglésAntioxidants, 13 (12), 1440.PID2022-143279OB-100PID2021-123564OB-100PDC2023-145806-100PID2020-115091RB-I00RED2022-134786-TPMP22/00100PI22/004752021-SGR00490US-1262734P20-00843JDC2022-048952-I2022 INV-1 00065https://doi.org/10.3390/antiox13121440info:eu-repo/semantics/openAccessoai:idus.us.es:11441/1705342026-06-17T12:51:07Z |
| dc.title.none.fl_str_mv |
Neuroinflammation in Age-Related Neurodegenerative Diseases: Role of Mitochondrial Oxidative Stress |
| title |
Neuroinflammation in Age-Related Neurodegenerative Diseases: Role of Mitochondrial Oxidative Stress |
| spellingShingle |
Neuroinflammation in Age-Related Neurodegenerative Diseases: Role of Mitochondrial Oxidative Stress Abadin, X. Cuproptosis Ferroptosis Inflammasomes Mitochondria Mitochondrial oxidative stress Necroptosis Neuroinflammation Pyroptosis |
| title_short |
Neuroinflammation in Age-Related Neurodegenerative Diseases: Role of Mitochondrial Oxidative Stress |
| title_full |
Neuroinflammation in Age-Related Neurodegenerative Diseases: Role of Mitochondrial Oxidative Stress |
| title_fullStr |
Neuroinflammation in Age-Related Neurodegenerative Diseases: Role of Mitochondrial Oxidative Stress |
| title_full_unstemmed |
Neuroinflammation in Age-Related Neurodegenerative Diseases: Role of Mitochondrial Oxidative Stress |
| title_sort |
Neuroinflammation in Age-Related Neurodegenerative Diseases: Role of Mitochondrial Oxidative Stress |
| dc.creator.none.fl_str_mv |
Abadin, X. Dios, Cristina de Zubillaga, M. Ivars, E. Puigròs, M. Marí, M. Morales, A. Vizuete Chacón, María Luisa Vitorica Ferrández, Francisco Javier Trullas, R. Colell, A. Roca Agujetas, Vicente |
| author |
Abadin, X. |
| author_facet |
Abadin, X. Dios, Cristina de Zubillaga, M. Ivars, E. Puigròs, M. Marí, M. Morales, A. Vizuete Chacón, María Luisa Vitorica Ferrández, Francisco Javier Trullas, R. Colell, A. Roca Agujetas, Vicente |
| author_role |
author |
| author2 |
Dios, Cristina de Zubillaga, M. Ivars, E. Puigròs, M. Marí, M. Morales, A. Vizuete Chacón, María Luisa Vitorica Ferrández, Francisco Javier Trullas, R. Colell, A. Roca Agujetas, Vicente |
| author2_role |
author author author author author author author author author author author |
| dc.contributor.none.fl_str_mv |
Bioquímica y Biología Molecular Ministerio de Ciencia e Innovación (MICIN). España Instituto de Salud Carlos III Generalitat de Catalunya Junta de Andalucía Agencia Estatal de Investigación. España European Union (UE) |
| dc.subject.none.fl_str_mv |
Cuproptosis Ferroptosis Inflammasomes Mitochondria Mitochondrial oxidative stress Necroptosis Neuroinflammation Pyroptosis |
| topic |
Cuproptosis Ferroptosis Inflammasomes Mitochondria Mitochondrial oxidative stress Necroptosis Neuroinflammation Pyroptosis |
| description |
A shared hallmark of age-related neurodegenerative diseases is the chronic activation of innate immune cells, which actively contributes to the neurodegenerative process. In Alzheimer’s disease, this inflammatory milieu exacerbates both amyloid and tau pathology. A similar abnormal inflammatory response has been reported in Parkinson’s disease, with elevated levels of cytokines and other inflammatory intermediates derived from activated glial cells, which promote the progressive loss of nigral dopaminergic neurons. Understanding the causes that support this aberrant inflammatory response has become a topic of growing interest and research in neurodegeneration, with high translational potential. It has been postulated that the phenotypic shift of immune cells towards a proinflammatory state combined with the presence of immunogenic cell death fuels a vicious cycle in which mitochondrial dysfunction plays a central role. Mitochondria and mitochondria-generated reactive oxygen species are downstream effectors of different inflammatory signaling pathways, including inflammasomes. Dysfunctional mitochondria are also recognized as important producers of damage-associated molecular patterns, which can amplify the immune response. Here, we review the major findings highlighting the role of mitochondria as a checkpoint of neuroinflammation and immunogenic cell deaths in neurodegenerative diseases. The knowledge of these processes may help to find new druggable targets to modulate the inflammatory response. |
| publishDate |
2024 |
| dc.date.none.fl_str_mv |
2024 |
| dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
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article |
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publishedVersion |
| dc.identifier.none.fl_str_mv |
https://hdl.handle.net/11441/170534 https://doi.org/10.3390/antiox13121440 |
| url |
https://hdl.handle.net/11441/170534 https://doi.org/10.3390/antiox13121440 |
| dc.language.none.fl_str_mv |
Inglés |
| language_invalid_str_mv |
Inglés |
| dc.relation.none.fl_str_mv |
Antioxidants, 13 (12), 1440. PID2022-143279OB-100 PID2021-123564OB-100 PDC2023-145806-100 PID2020-115091RB-I00 RED2022-134786-T PMP22/00100 PI22/00475 2021-SGR00490 US-1262734 P20-00843 JDC2022-048952-I 2022 INV-1 00065 https://doi.org/10.3390/antiox13121440 |
| dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess |
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openAccess |
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application/pdf application/pdf |
| dc.publisher.none.fl_str_mv |
Multidisciplinary Digital Publishing Institute (MDPI) |
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Multidisciplinary Digital Publishing Institute (MDPI) |
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reponame:idUS. Depósito de Investigación de la Universidad de Sevilla instname:Universidad de Sevilla (US) |
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Universidad de Sevilla (US) |
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idUS. Depósito de Investigación de la Universidad de Sevilla |
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idUS. Depósito de Investigación de la Universidad de Sevilla |
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