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Parkinson's disease: connecting mitochondria to inflammasomes.
Lawrence, Grace M E P; Holley, Caroline L; Schroder, Kate.
Afiliação
  • Lawrence GMEP; Institute for Molecular Bioscience (IMB) Centre for Inflammation and Disease Research, University of Queensland, St Lucia, QLD, Australia.
  • Holley CL; Institute for Molecular Bioscience (IMB) Centre for Inflammation and Disease Research, University of Queensland, St Lucia, QLD, Australia.
  • Schroder K; Institute for Molecular Bioscience (IMB) Centre for Inflammation and Disease Research, University of Queensland, St Lucia, QLD, Australia. Electronic address: K.Schroder@imb.uq.edu.au.
Trends Immunol ; 43(11): 877-885, 2022 11.
Article em En | MEDLINE | ID: mdl-36229358
ABSTRACT
Activated microglia foster a neurotoxic, inflammatory environment in the mammalian central nervous system (CNS) that drives the pathology of neurodegenerative diseases including Parkinson's disease (PD). Moreover, mitochondrial fission promotes microglial inflammatory responses in vitro. Given that the NLRP3 inflammasome and mitochondria are central regulators of both inflammation and PD, we explore potential functions for the NLRP3 inflammasome and mitochondrial dynamics in PD. Specifically, we propose that inducible microglial mitochondrial fission can promote NLRP3-dependent neuroinflammation in hereditary and idiopathic PD. Further in-depth exploration of this topic can prompt valuable discoveries of the underlying molecular mechanisms of PD neuroinflammation, identify novel candidate anti-inflammatory therapeutics for PD, and ideally provide better outcomes for PD patients.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Doença de Parkinson / Inflamassomos Limite: Animals / Humans Idioma: En Revista: Trends Immunol Ano de publicação: 2022 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Doença de Parkinson / Inflamassomos Limite: Animals / Humans Idioma: En Revista: Trends Immunol Ano de publicação: 2022 Tipo de documento: Article