Your browser doesn't support javascript.
loading
Heme oxygenase-1: The roles of both good and evil in neurodegenerative diseases.
Liu, Rong; Yang, Jiahua; Li, Yinghui; Xie, Junxia; Wang, Jun.
Afiliação
  • Liu R; School of Basic Medicine, Qingdao University, Qingdao, China.
  • Yang J; Institute of Brain Science and Disease, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders, Qingdao University, Qingdao, China.
  • Li Y; School of Basic Medicine, Qingdao University, Qingdao, China.
  • Xie J; Institute of Brain Science and Disease, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders, Qingdao University, Qingdao, China.
  • Wang J; School of Basic Medicine, Qingdao University, Qingdao, China.
J Neurochem ; 167(3): 347-361, 2023 Nov.
Article em En | MEDLINE | ID: mdl-37746863
ABSTRACT
Heme oxygenase-1 (HO-1) is the only way for cells to decompose heme. It can cleave heme to produce carbon monoxide (CO), ferrous iron (Fe2+ ), and biliverdin (BV). BV is reduced to bilirubin (BR) by biliverdin reductase(BVR). In previous studies, HO-1 was considered to have protective effects because of its anti-inflammatory, anti-apoptosis, and antiproliferation functions. However, emerging experimental studies have found that the metabolites derived from HO-1 can cause increase iin intracellular oxidative stress, mitochondrial damage, iron death, and autophagy. Because of its particularity, it is very meaningful to understand its exact mechanism. In this review, we summarized the protective and toxic effects of HO-1, its potential mechanism, its role in neurodegenerative diseases and related drug research. This knowledge may be beneficial to the development of new therapies for neurodegenerative diseases and is crucial to the development of new therapeutic strategies and biomarkers.
Palavras-chave

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2023 Tipo de documento: Article