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. 2019 May 2;2019:1743183. doi: 10.1155/2019/1743183

Figure 2.

Figure 2

miRNAs that indirectly impact α-syn without binding to its 3′-UTR. Several miRNAs cause impairment of the chaperone-mediated autophagy (CMA) and autophagy-lysosome network (ALN) pathways, leading to α-syn accumulation. Lamp2a in the CMA pathway is targeted by miR-21∗, miR-224, miR-373∗, and miR-379, while Hsc70 is targeted by miR-26b, miR-106a∗, miR-301b, and probably miR-320a and miR-16-1. In the ALN, TFEB, which is necessary for lysosomal biogenesis and function, is directly targeted and reduced by miR-128. Let-7, on the other hand, can suppress lgg-1 and atg-13. Therefore, miR-128 and let-7 contribute to PD pathogenesis by impairing the ALN. On the other hand, SIAH1, a monoubiquitylation modifier of α-syn, is inhibited by miR-15b-5p, leading to decreased α-syn aggregation. Moreover, lncRNA SNHG1 could directly bind miR-15-5p and repress miR-15-5p expression. The roles of miR-133b and miR-433 are controversial. miR-133b may inhibit α-syn expression via inhibition of RhoA, while miR-433 may suppress α-syn expression via FGF20 inhibition.