Abstract
Silence information regulator 1 (SIRT1), a member of the sirtuin family, targets histones and many non-histone proteins and participates in various physiological functions. The enzymatic activity of SIRT1 is decreased in patients with Parkinson’s disease (PD), which may reduce their ability to resist neuronal damage caused by various neurotoxins. As far as we know, SIRT1 can induce autophagy by regulating autophagy related proteins such as AMP-activated protein kinase, light chain 3, mammalian target of rapamycin, and forkhead transcription factor 1. Furthermore, SIRT1 can regulate mitochondrial function and inhibit oxidative stress mainly by maintaining peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) in a deacetylated state and thus maintaining a constant level of PGC-1α. Other studies have demonstrated that SIRT1 may play a role in the pathophysiology of PD by regulating neuroinflammation. SIRT1 deacetylases nuclear factor-kappa B and thus reduces its transcriptional activity, inhibits inducible nitric oxide synthase expression, and decreases tumor necrosis factor-alpha and interleukin-6 levels. SIRT1 can also upregulate heat shock protein 70 by deacetylating heat shock factor 1 to increase the degradation of α-synuclein oligomers. Few studies have focused on the relationship between SIRT1 single nucleotide polymorphisms and PD risk, so this topic requires further research. Based on the neuroprotective effects of SIRT1 on PD, many in vitro and in vivo experiments have demonstrated that some SIRT1 activators, notably resveratrol, have potential neuroprotective effects against dopaminergic neuronal damage caused by various neurotoxins. Thus, SIRT1 plays a critical role in PD development and might be a potential target for PD therapy.
Highlights
Parkinson's disease (PD) is a progressive neurodegenerative disease of the central nervous system (CNS)
Based on the neuroprotective effects of Silence information regulator 1 (SIRT1) on PD, many in vitro and in vivo experiments have demonstrated that some SIRT1 activators, notably resveratrol, have potential neuroprotective effects against dopaminergic neuronal damage caused by various neurotoxins
The results indicated that the mean protein level of 120 kDa SIRT1 in the frontal cortex was 28% lower in patients with PD than in controls (P
Summary
Parkinson's disease (PD) is a progressive neurodegenerative disease of the central nervous system (CNS). Studies into neurodegenerative diseases have found that SIRT1 can reduce the degeneration of human nucleus pulposus cells by inducing autophagy [49, 50]. We showed that the activation of SIRT1 by resveratrol led to the redistribution of LC3 from the nucleus into the cytoplasm, which was accompanied by an increase in LC3-II expression and the autophagic degradation of α-synuclein and p62 in DA neurons.
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