Table 1.
The miRNAs with verified functions in ASD. In the column of Change in ASD, “↑”, “↓”, and “↕” mean up-regulation, down-regulation, and inconsistent change, respectively.
| miRNA | Change in ASD | Target | Function | References |
|---|---|---|---|---|
| miR-21-3p | ↑ | PAFAH1B1/LIS1,DYNC1I1 | miR-21-3p inhibits the PAFAH1B1/LIS1 and DYNC1I1 genes of M16 mRNA module, which is related to neuronal migration and synapses of ASD | [24,61] |
| miR-21-5p | ↑ | OXTR | miR-21-5p inhibits OXTR translation which may aggravate ASD phenotype | [68] |
| miR-29b | ↑ | COL6A2, ID3 | The inhibition of COL6A2 caused by the up-regulation of miR-29b is one of the underlying genetic mechanisms of ASD muscle disease and dyskinesia; miR-29b targets the ID3 gene. In addition, miR-29b is related to circadian rhythm signals, and studies have reported that ASD is associated with circadian rhythm disturbances | [59] |
| miR-103a-3p | ↕ | BDNF | miR-103a-3p targets the brain-derived neurotrophic factor (BDNF) gene, BDNF is directly or indirectly involved in ASD, and BDNF plays a key role in neuronal differentiation and synapses | [69] |
| miR-146a | ↑ | GRIA3, MAP1B, KCNK2 |
miR-146a inhibits MAP1B, GRIA3, and KCNK2, therefore impairing ASD synaptic transmission and inhibiting neuronal migration; miR-146a contributes to neuroinflammation of ASD patients | [53,70] |
| miR-153 | ↓ | LEPR | The expression of miR-153 is reduced in ASD mouse models, and miR-153 activates the janus kinase-signal transducer and activator of transcription ( JAK-STAT ) signaling pathway by directly increasing leptin receptor ( LEPR), and finally attenuating the symptoms of ASD in mice | [71] |
| miR-219 | ↓ | PLK2 | miR-219 can directly target PLK2, and PLK2 overexpression may lead to an overall reduction in synaptic strength and neuronal excitability, which may lead to synaptic dysfunction in ASD | [59] |
| miR-221 | ↓ | FMR1 | miR-221 represses FMR1 at the synapse | [70,72] |
| miR-486-3p | ↑ | ARID1B | miR-486-3p can directly target ARID1B, and the mutation of ARID1B may increase the risk of ASD | [73,74,75,76] |
| hsa_can_1002-m | ↓ | EPS8, ADAM12, CHUK, RUNX1 | hsa_can_1002-m activates epidermal growth factor receptor (EGFR) and fibroblast growth factor receptor (FGFR) signaling pathways in the ASD cortex by targeting EPS8, ADAM12, CHUK, and RUNX1. The EGFR and FGFR signaling pathways may play a potential role in the molecular pathology of ASD | [24] |