The Role of Non-coding RNAs in Methamphetamine-Induced Neurotoxicity.
Luyao XuLingyue LiQianling ChenYuebing HuangXuebing ChenDongfang QiaoPublished in: Cellular and molecular neurobiology (2023)
Methamphetamine (METH) is an amphetamine-type stimulant that is highly toxic to the central nervous system (CNS). Repeated intake of METH can lead to addiction, which has become a globalized problem, resulting in multiple public health and safety problems. Recently, the non-coding RNA (ncRNA) has been certified to play an essential role in METH addiction through various mechanisms. Herein, we mainly focused on three kinds of ncRNAs including long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs), which are involved in neurotoxicity effects such as cognitive impairment, behavioral abnormalities, and psychiatric disorders due to METH abuse. In addition, differential expression (DE) ncRNAs also suggest that specific responses and sensitivity to METH neurotoxicity exist in different brain regions and cells. We summarized the relationships between the ncRNAs and METH-induced neurotoxicity and psychiatric disturbances, respectively, hoping to provide new perspectives and strategies for the prevention and treatment of METH abuse. Schematic diagram of the non-coding RNAs (ncRNAs) was involved in methamphetamine (METH)-induced neurotoxicity. The ncRNAs were involved in METH-induced blood-brain barrier disruption, neuronal, astrocyte, and microglial damage, and synaptic neurotransmission impairment. The study of ncRNAs is a hot spot in the future to further understand the neurotoxicity of METH and provide more favorable scientific support for clinical diagnosis and innovation of related treatments.
Keyphrases
- blood brain barrier
- public health
- high glucose
- diabetic rats
- long non coding rna
- cognitive impairment
- mental health
- cerebral ischemia
- induced apoptosis
- attention deficit hyperactivity disorder
- endothelial cells
- cell proliferation
- physical activity
- signaling pathway
- spinal cord
- weight loss
- lipopolysaccharide induced
- subarachnoid hemorrhage
- cell cycle arrest
- weight gain
- brain injury
- lps induced
- endoplasmic reticulum stress