microRNAs: Emerging Targets Regulating Oxidative Stress in the Models of Parkinson's Disease

Abstract

Parkinson's disease (PD) is the second most common neurodegenerative disorder. This chronic, progressive disease is characterized by loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) and the presence of cytoplasmic inclusions called Lewy bodies (LBs) in surviving neurons. PD is attributed to a combination of environment and genetic factors, but the precise underlying molecular mechanisms remain elusive. Oxidative stress is generally recognized as one of the main causes of PD, and excessive reactive oxygen species (ROS) can lead to DA neuron vulnerability and eventual death. Several studies have demonstrated that small non-coding RNAs termed microRNAs (miRNAs) can regulate oxidative stress in vitro and in vivo models of PD. Relevant miRNAs involved in oxidative stress can prevent ROS-mediated damage to DA neurons, suggesting that specific miRNAs may be putative targets for novel therapeutic targets in PD.

Keywords: Nrf2; Parkinson's disease; microRNAs; mitochondrial dysfunction; oxidative stress; α-synuclein.

Figure 1

Schematic model depicting the role of miRNAs regulating oxidative stress in PD. Activation steps are represented by solid lines and inhibitory effects are represented by dashed lines.