Research progress on the mechanism of PGC-1α, a key regulator of mitochondrial biogenesis, in arsenic-induced nervous system damage
10.3760/cma.j.cn231583-20220517-00173
- VernacularTitle:线粒体生物发生关键调控因子PGC-1α在砷致神经系统损伤中作用机制的研究进展
- Author:
Xinbo MA
1
;
Xiaona LIU
;
Yanmei YANG
Author Information
1. 哈尔滨医科大学中国疾病预防控制中心地方病控制中心慢性病防治中心，哈尔滨 150081
- Keywords:
Arsenic;
Neurotoxicity;
PGC-1α;
Nervous system
- From:
Chinese Journal of Endemiology
2024;43(2):157-160
- CountryChina
- Language:Chinese
-
Abstract:
Arsenic, as a toxic substance that can affect human health, can cause various neurological disorders, including cognitive impairment, when excessive. Relevant epidemiological surveys and animal experimental studies have shown that exposure to arsenic can not only cause intellectual impairment and peripheral neuropathy in humans, but also lead to abnormal behavior in humans and animals. However, so far, the mechanism of arsenic induced damage to the nervous system is still unclear. Peroxisome proliferator activated receptor γ auxiliary activation factor 1α (PGC-1α), as a nuclear transcription coactivator, can interact with transcription factors or other coactivators and plays a role in biological processes such as mitochondrial biogenesis and energy metabolism. PGC-1α, by activating mitochondrial biogenesis, affecting energy metabolism, activating oxidative stress regulatory factors [catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), etc.], mitigates the damage to the central nervous system (CNS), peripheral nervous system (PNS), and blood-brain barrier (BBB) caused by arsenic. This article summarize the research progress of arsenic-induced neurological injury and the mechanism of PGC-1α's role in arsenic-induced neurological injury to provide a theoretical basis for further prevention and treatment of neurological diseases caused by arsenic.
