Table 3.
Disease 2 | Model | Pathomechanism Modifying Effects | Related Factors 3 | References |
---|---|---|---|---|
AD | Aβ25–35-treated SH-SY5Y and HPN cells | miR-137-3p represses KREMEN1 and has a positive effect on pathology by contributing to increased cell viability, reduced apoptosis, and increased mitochondrial membrane potential. | SNHG1, SNHG19, KREMEN1 | [48,55] |
Aβ1–42-treated SH-SY5Y cells and chemically induced AD mice | miR-137-5p reduces Aβ deposition, tau phosphorylation, and apoptosis by downregulating USP30. | USP30 | [44,51] | |
APP/PS1 double-transgenic AD mice | Downregulation of miR-137 coincides with upregulation of its target, CACNA1C. | CACNA1C | [51] | |
AD patient cortex, TgCRND8 mice | miR-137 protects against high-fat diet-related AD risk by suppressing serine palmitoyltransferase expression that leads to lowered Aβ levels. | SPTLC1 | [37,60] | |
propofol-treated rats and SK-N-SH cells | miR-137-3p reduces neuronal apoptosis and restores cell proliferation by suppressing the proinflammatory neurotrophic factor PTN. | PTN | [50] | |
streptozotocin-treated rats | miR-137-3p ameliorates memory impairment by downregulating MAGL (monoacylglycerol lipase), an endocannabinoid-degrading enzyme. | MAGL | [49] | |
PD | MPP+-induced SH-SY5Y cell model | Suppression of miR-137-3p by OIP5-AS1 leads to upregulation of the mitophagy receptor NIX, which contributes to reduced ROS levels and normalization of the mitochondrial membrane potential. | OIP5-AS1, NIX | [52] |
MPP+-induced rat primary neuronal cell | miR-137-3p decreases OXR1 levels and increases oxidative damage and apoptosis. | OXR1 | [53] | |
α-synuclein A30P-expressing Drosophila | Several neurotransmitter receptor targets of upregulated miR-137-3p are downregulated. | D2R, GABA-B-R3, Nmdar2 | [75] | |
HD | HEK293T cells | miR-137-3p negatively regulates HTT translation. | HTT | [54] |
murine Hdh109/109 striatal cells | miR-137 is involved in REST-dependent transcriptional dysregulation. | REST | [85] |
1 The table contains pathomechanisms that were experimentally explored/validated in the specific disorders. 2 AD: Alzheimer’s disease, PD: Parkinson’s disease, and HD: Huntington’s disease. 3 ceRNA names are underlined.