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Mitochondria Regulate Inflammatory Paracrine Signalling in Neurodegeneration.
Faccenda, Danilo; Campanella, Michelangelo.
Afiliação
  • Faccenda D; Department of Comparative Biomedical Sciences, The Royal Veterinary College, University of London, Royal College Street, London, NW1 0TU, UK.
  • Campanella M; Department of Comparative Biomedical Sciences, The Royal Veterinary College, University of London, Royal College Street, London, NW1 0TU, UK. mcampanella@rvc.ac.uk.
J Neuroimmune Pharmacol ; 15(4): 565-566, 2020 12.
Article em En | MEDLINE | ID: mdl-32915348
Mitochondrial dysfunction occurs in most neurodegenerative diseases, contributing to both their onset and progression. A recent breakthrough unveiled that propagation of the inflammatory response and subsequent neuronal injury are also mediated extracellularly by damaged mitochondria, which are released from active microglial cells into the brain milieu. These extracellular fragmented mitochondria can therefore generate sufficient toxicity to trigger neuronal death and widespread brain damage through activation of naïve astrocytes. Besides suggesting potential new pharmacological strategies of therapeutic intervention in neurodegeneration, this original work indicates that mitochondria might act as bioactive ligands exerting paracrine functions. This is an interesting, novel and impactful concept that deserves consideration by the scientific community, as the attention should now be focused on the identification of the specific receptors through which mitochondria mediate such an important extracellular signalling mechanism in neurological conditions.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Transdução de Sinais / Mediadores da Inflamação / Doenças Neurodegenerativas / Comunicação Parácrina / Mitocôndrias Limite: Humans Idioma: En Ano de publicação: 2020 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Transdução de Sinais / Mediadores da Inflamação / Doenças Neurodegenerativas / Comunicação Parácrina / Mitocôndrias Limite: Humans Idioma: En Ano de publicação: 2020 Tipo de documento: Article