The role of heat shock protein B8 in neuronal protection against oxidative stress and mitochondrial dysfunction: A literature review.
Int Immunopharmacol
; 140: 112836, 2024 Oct 25.
Article
em En
| MEDLINE
| ID: mdl-39094362
ABSTRACT
Excessive oxidative stress triggers cerebrovascular and neurodegenerative diseases resulting in acute and chronic brain injury. However, the underlying mechanisms remain unknown. Levels of small heat shock protein B8 (HSPB8), which is highly expressed in the brain, are known to be significantly elevated in cerebral injury models. Exogenous HSPB8 protects the brain against mitochondrial damage. One potential mechanism underlying this protection is that HSPB8 overexpression alleviates the mitochondria-dependent pathways of apoptosis; mitochondrial biogenesis, fission, and mitophagy. Overexpression of HSPB8 may therefore have potential as a clinical therapy for cerebrovascular and neurodegenerative diseases. This review provides an overview of advances in the protective effects of HSPB8 against excessive cerebral oxidative stress, including the modulation of mitochondrial dysfunction and potent signaling pathways.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Estresse Oxidativo
/
Proteínas de Choque Térmico
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Mitocôndrias
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Neurônios
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Int Immunopharmacol
/
Int. immunopharmacol
/
International immunopharmacology
Assunto da revista:
ALERGIA E IMUNOLOGIA
/
FARMACOLOGIA
Ano de publicação:
2024
Tipo de documento:
Article
País de afiliação:
China