Mitochondria-induced immune response as a trigger for neurodegeneration : A pathogen from within
Luna-Sánchez, Marta (Universitat Autònoma de Barcelona. Departament de Biologia Cel·lular, de Fisiologia i d'Immunologia)
Bianchi, Patrizia (Universitat Autònoma de Barcelona. Institut de Neurociències)
Quintana Romero, Albert (Universitat Autònoma de Barcelona. Departament de Biologia Cel·lular, de Fisiologia i d'Immunologia)

Fecha:	2021
Resumen:	Symbiosis between the mitochondrion and the ancestor of the eukaryotic cell allowed cellular complexity and supported life. Mitochondria have specialized in many key functions ensuring cell homeostasis and survival. Thus, proper communication between mitochondria and cell nucleus is paramount for cellular health. However, due to their archaebacterial origin, mitochondria possess a high immunogenic potential. Indeed, mitochondria have been identified as an intracellular source of molecules that can elicit cellular responses to pathogens. Compromised mitochondrial integrity leads to release of mitochondrial content into the cytosol, which triggers an unwanted cellular immune response. Mitochondrial nucleic acids (mtDNA and mtRNA) can interact with the same cytoplasmic sensors that are specialized in recognizing genetic material from pathogens. High-energy demanding cells, such as neurons, are highly affected by deficits in mitochondrial function. Notably, mitochondrial dysfunction, neurodegeneration, and chronic inflammation are concurrent events in many severe debilitating disorders. Interestingly in this context of pathology, increasing number of studies have detected immune-activating mtDNA and mtRNA that induce an aberrant production of pro-inflammatory cytokines and interferon effectors. Thus, this review provides new insights on mitochondria-driven inflammation as a potential therapeutic target for neurodegenerative and primary mitochondrial diseases.
Ayudas:	European Research Council ERC-2014-StG-638106 Ministerio de Economía y Competitividad SAF2014-57981P Agencia Estatal de Investigación SAF2017-88108-R "la Caixa" Foundation 100010434 Agència de Gestió d'Ajuts Universitaris i de Recerca 2017SGR- 323 Ministerio de Economía y Competitividad SAF2017-88108-R
Nota:	Funding: This work was supported by a Juan de la Cierva grant (IJC2018-036938-I). A.Q. received funds from the European Research Council (Starting grant NEUROMITO, ERC-2014-StG-638106), MINECO Proyectos I + D de Excelencia (SAF2014-57981P; SAF2017-88108-R), AGAUR (2017SGR- 323), and "la Caixa" Foundation (ID 100010434), under the agreement LCF/PR/HR20/52400018.
Nota:	This work was supported by a Juan de la Cierva grant (IJC2018?036938?I). A.Q. received funds from the European Research Council (Starting grant NEUROMITO, ERC?2014?StG?638106), MINECO Proyectos I + D de Excelencia (SAF2014?57981P; SAF2017?88108?R), AGAUR (2017SGR? 323), and ?la Caixa? Foundation (ID 100010434), under the agreement LCF/PR/HR20/52400018.
Nota:	Altres ajuts: NEUROMITO
Nota:	Altres ajuts: "la Caixa" Foundation
Derechos:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Lengua:	Anglès
Documento:	Article ; recerca ; Versió publicada
Materia:	MtDNA ; MtRNA ; Mitochondrial dysfunction ; Mitochondrial disorders ; Neurodegeneration ; Antiviral response ; Inflammation ; Innate immunity ; Interferon
Publicado en:	International journal of molecular sciences, Vol. 22 Núm. 16 (August 2021) , p. 8523, ISSN 1422-0067

DOI: 10.3390/ijms22168523
PMID: 34445229

19 p, 1.9 MB

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