Table 2.
MiRs and their involvement in OA-related apoptosis.
| Apoptosis | Induced Effect | Signaling Pathway | Reference No. |
|---|---|---|---|
| miR-195-5p | mRNA and protein levels of IL-1β, IL-6 and TNF-α were significantly enhanced | mir-195-5p activated the lPS-induced repression of the Wnt/β-catenin signaling pathway and activation of the nuclear factor (NF)-κB signaling pathway in ATDC5 cells | [5] |
| miR-335-5p | significantly reduces the expression of inflammatory factors (IL-1β, IL-6, and TNF-α) | significantly enhanced expression levels of the autophagy-related genes encoding the autophagy-related proteins Beclin-1, ATG5, and ATG7 | [6] |
| miR-9 | reduces the IL-1β mediated production of TNF-α and reduces basal and IL-1β-induced MMP13 protein release | PXR/RXR activation, G-protein coupled receptor (GPCR) signaling and Wnt/b-catenin signaling | [7] |
| miR-145 | miR-145 up-regulation decreases LPS-induced inflammatory injury in ATDC5 cells through SAL | functioned in LPS-induced injury by blocking NF-κB and p38MAPK signaling pathways | [9] |
| miR-337-3p | - | miR-337-3p in OA increased PTEN expression and thus PI3K/AKT signaling pathway was blocked by PTEN | [13] |
| miR-27b-3p | TNF-αand IL-6 levels repressed by the silencing of PVT1 were significantly enhanced by knockdown of miR-27b-3p in C28/I2 cells treated by IL-1β | miR-27b-3p decreased cell viability that was promoted by the silencing of PVT1 in IL-1β-treated C28/I2 cells, miR-27b-3p abrogated the promoting effect of PVT1 knockdown on autophagy in C28/I2 cells challenged by IL-1β | [20] |
| miR-125b | - | miR-125b noticeably alleviated the LPS+pc-THRIL-induced JAK1/STAT3 and NF-κB pathways activation | [23] |
| miR-26a-5p | - | - | [24] |
| miR-107 | - | miR-107 inhibited the activation of AKT/mTOR and NF-κB pathway | [25] |
| miR-218-5p | - | The expression of PIK3C2A, Akt, mTOR and S6 was downregulated, while 24 4EBP1 was upregulated | [26] |
| miR-222 | - | - | [27] |
| miR-140-5p | miR-140-5p reduced the expression of HMGB1 protein, p-AKT (Ser473) and p-PI3K in IL-1β-induced chondrocytes | inhibited the PI3K/ AKT signaling pathway and suppressed the progression of OA through targeting HMGB1 | [28] |
| miR-1236 | - | miR-1236 overexpression promotes OA by inhibiting proliferation and induces apoptosis of chondrocytes, partially through PIK3R3 repression. | [29] |
| miR-26b | - | - | [30] |
| miR-93-5p | Overexpression of miR-93-5p was found to significantly inhibit IL-1β–induced chondrocyte apoptosis. In general, IL-1β enhances the expression of matrix-degrading enzymes (MMP3 and MMP13), which in turn degrade the ECM | miR-93-5p exerted its actions in chondrocytes partially through suppression of TCF4 expression | [31] |
| miR-675-3p | miR-675-3p overexpression inhibited the IL-6 and IL-8 expression that was caused by IL-1b stimulation | miR-675-3p mimic markedly attenuated the increase in the GNG5 expression levels | [32] |
| miR-29b | - | - | [33] |
| miR-455-3p | miR-455-3p significantly inhibited the viability of CHON-001 cells IL-1β-induced apoptosis of CHON-001 was significantly increased by up-regulation of miR-455-3p | miR-455-3p directly regulated COL2A1 expression through binding its 3′UTR sequence | [34] |
| miR-142-5p | miR-142-5p overexpression resulted in significantly decreased levels of IL-1β and TNF-α and increased levels of IL-10 | miR-142-5p overexpression downregulated CXCR4 expression | [35] |
The bold font style designates miRs with the most significant dysregulation between patients and controls across multiple studies (correlated).