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. 2024 Jun 30;25(13):7229. doi: 10.3390/ijms25137229

Table 3.

Pathomechanisms affected by miR-137 in neurodegenerative disorders 1.

Disease 2 Model Pathomechanism Modifying Effects Related Factors 3 References
AD 25–35-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]
1–42-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.