Table 1.
Studies that summarized the involvement of lncRNAs in hypoxic/anoxic conditions.
| Studies that Summarized the Involvement of LncRNAs SNHG Family in Hypoxic/Anoxic Conditions | |||
| SH-SY5Y OGD/R-induced | SNHG1 | The overexpression of SNHG1 or the KO of miR-140-5p alleviated hypoxia-induced damage. Overall, the results proved that lncRNA SNHG1 could be novel therapeutic target in hypoxic brain injury | [63] |
| Primary BMEC mice OGD/R-induced | SNHG1 | Snhg1 silencing led to worsening the BMEC apoptosis that was OGD/R-induced, so confirmed the protective effect of lncRNA Snhg1in in IS model | [64] |
| C57Bl/6 mice with ligation of the right internal carotid artery. Primary hippocampal cell culture with shRNA or miRNA mimic transfection |
SNHG3 | Snhg3 silencing led to reduction in cell viability and promoted the apoptosis, in vivo Snhg3 overexpression improved brain neurological function in the animals and reduced HIBD |
[65] |
| OGD/R-induced primary neurons | SNHG12 | SNHG12 knockdown exacerbated apoptosis induced by OGD/R | [66] |
| HT22 cells of I/R model | SNHG12 | SNHG12 increased cell activity and inhibited oxidative stress through inhibition of SIRT1/FOXO3a signaling-mediated autophagy | [67] |
| N2A cells ODG/R-induced MCAO/R mice |
SNHG14 | SNHG14 silencing led to an increase in miR-98-5p and BCL2L13 depletion. So, SNHG14 is beneficial to OGD/R | [68] |
| MCAO male SD rats OGD-induced primary cortical neurons of SD embryos rat |
SNHG14 | SNHG14 silencing led to a reduction in the infarct volume and improved neurological deficits in MCAO rats | [69] |
| H/I mice model PC12 cells OGD-stimulated |
SNHG15 | SNHG15 suppression alleviated H/I brain injury by modulating the miR-153-3p/SETD7 axis | [70] |
| HBMECs OGD/R-induced | SNHG16 | The overexpression of SNHG16 led to a decrease in miR-15a-5p and increased the Bcl-2 expression levels, as well as reduced apoptosis and enhanced cell survival | [71] |
| Studies that Summarized the Involvement of LncRNA MALAT1 In Hypoxic/Anoxic Conditions | |||
| C57BL/6 mice with right common carotid artery occlusion C57BL/6 mice hippocampal neurons with H/I |
MALAT1 | MALAT1 acting as a miR-429 sponge led to an increment in WNT1 expression promoting apoptosis, as shown by expression levels of cleaved caspase-3 and the ratio of Bax to Bcl-2 both in vitro and vivo | [72] |
| HBMECs OGD-induced | MALAT1 | Through sponging miR-126, MALAT1 inhibited proliferation and induced apoptosis of OGD-induced HBMECs | [73] |
| bEnd.3 OGD-induced | MALAT1 | The MALAT1-miR-200c-3p-SIRT1 pathway could be interesting to modulate for influencing autophagy and cell survival for neuroprotection | [74] |
| BMECs of C57BL/6J mice OGD/R-induced | MALAT1 | MALAT1 increased autophagy and cell survival in BMECs | [75] |
| MCAO mice BMECs OGD-induced |
MALAT1 | MALAT1 interactions reduced cell death and inflammation | [76] |
| MCAO C57BL/6J mice BMECs OGD/R-induced |
MALAT1 | Following OGD/R, MALAT1 regulated angiogenesis | [77] |
| Studies that Summarized the Involvement of LncRNA H19 In Hypoxic/Anoxic Conditions | |||
| Neonatal HIE SD rats | H19 | H19 overexpression reduced both the nervous damage and autophagy of brain tissue, as well as improved neurological functions | [78] |
| Primary neuron cells rat OGD-induced HIBD SD rat induced by partial occlusion of carotid artery |
H19 | HIBD can be prevented by overexpression of the lncRNA H19 | [79] |
| HIBD neonatal rats | H19 | H19 overexpression suppressed apoptosis in rat cardiomyocytes | [80] |
| Blood samples of IS patients MCAO/R rats SH-SY5Y cells OGD-induced |
H19 | Hypoxia/ischemia-induced neuronal injury was attenuated by blocking the lncRNA H19-miR-19a-Id2 axis | [81] |
| PC-12 cells induced by hypoxia | H19 | Overexpression of lncRNA H19 led to an increase in cell damage induced by hypoxic conditions | [82] |
| IS patients MCAO mouse BV2 cell OGD-induced |
H19 | H19 could be a useful marker as well as a potential therapeutic target for IS patients | [83] |
| Studies that Summarized the Involvement of LncRNA GAS5 in Hypoxic/Anoxic Conditions | |||
| Blood of CA/CCR patients OGD/R-inducted astrocytes |
GAS5 | Inhibiting PI3K/Akt signaling through INPP4B, lncRNAGAS5/miR-137 is a hypoxia-responsive axis involved in astrocyte–microglia crosstalk. | [84] |
| HIBD neonatal rat model established and treated with shRNA-GAS5 or antagomir miR-128-3p | GAS5 | Through the microRNA-128-3p/Bax/Akt/GSK-3β axis, downregulation of GAS5 prevents mitochondrial apoptosis and HIBD in neonatal rats | [85] |
| Primary rat cortical cell hypoxia-treated B35 cell with hypoxic treated MCAO SD rats |
GAS5 | GAS5 can lead to worsening of cell apoptotic processes in hypoxic conditions targeting miR-221/PUMA axis. Consequently, GAS5 could be useful in ischemic stroke treatment | [86] |
| Studies that Summarized the Involvement of LncRNA NEAT1 in Hypoxic/Anoxic Conditions | |||
| BMECs OGD-induced | NEAT1 | NEAT1 facilitates survival and angiogenesis in OGD-induced BMECs via targeting miR-377 | [87] |
| Neonatal HIBD mouse model was established via right common carotid artery occlusion | NEAT1 | The findings demonstrated that NEAT1 alleviated HIBD in mice by binding to miR-339-5p | [88] |
| Studies that Summarized the Involvement of LncRNA MIAT in Hypoxic/Anoxic Conditions | |||
| Neuro2A cells OGD-induced Neonatal rat with permanent unilateral carotid ligation |
MIAT | The overexpression of MIAT reduced neuron apoptosis and relieved HI injury of neonatal rats through miR-211/GDNF | [89] |
| MCAO SD rats Primary rat neurons OGD/R- stimulated |
MIAT | MIAT exacerbated I/R injury by disrupting redox homeostasis in neurons | [90] |
| Studies that Summarized the Involvement of LncRNA PVT1 in Hypoxic/Anoxic Conditions | |||
| MCAO mice Primary neurons OGD/R-induced |
PVT1 | PVT1 silencing led to a reduction in infarct volume and improved neurological behavior in MCAO mice | [91] |
| HUVECs OGD-induced | PVT1 | PVT1 alleviated hypoxia-induced endothelial apoptosis by enhancing autophagy through the miR-15b-5p/ATG14 and miR-424-5p/ATG14 pathways | [92] |
| Studies that Summarized the Involvement of LncRNA Peg13 in Hypoxic/Anoxic Conditions | |||
| Neonatal HIBD mice Mouse hippocampal neurons OGD-induced |
PEG13 | Peg13 exerted an anti-apoptotic role, acting as a sponge for miR-20a-5p targeting XIAP | [93] |
| bEnd.3 cells OGD/R-induced MCAO mice |
PEG13 | Peg13 alleviated I/R-induced neurological deficit, cerebral infarct, and cerebral edema | [94] |
| Studies that Summarized the Involvement of LncRNA MEG3 in Hypoxic/Anoxic Conditions | |||
| PC12 cells induced by hypoxia | MEG3 | MEG3 silencing performed by siRNA played a neuroprotective function, preventing hypoxia-induced injury in PC12 via the modulation of protein involved in apoptosis and cell proliferation | [95] |
| MCAO C57BL/6J mice | MEG3 | Silencing MEG3 resulted in being protective against I/R-induced ischemic damage in vivo and improved overall neurological functions | [96] |
| PC12 cells cultivated in hypoxic conditions | MEG3 | MEG3 led to an increase in hypoxic damage in PC12 cells by targeting miR147 and the downstream target Sox2 | [97] |
| 260 neonatal female or male C57/BL6 mice with right cervical vessels ligated with a double bandage | MEG3 | MEG3 silencing improved the therapeutic effect of DEX on HIBD in neonatal mice through the expression of miR-129-5p | [98] |
| Studies that Summarized the Involvement of LncRNA BDNF-AS in Hypoxic/Anoxic Conditions | |||
| Mice received ligation of the unilateral common carotid artery Primary hippocampal neuron with hypoxic and oxidative stress induced |
BDNF-AS | Silenced BDNF-AS lncRNA attenuated HI events | [99] |
| HCN2 and human astrocytes after H/R | BDNF-AS | lncRNA BDNF-AS knockdown suppressed apoptosis | [100] |
OGD/R: oxygen-glucose deprivation/reperfusion; KO: knockout; BMEC: brain microvascular endothelial cells; IS: ischemic stroke; HIBD: hypoxic ischemic brain damage; I/R: ischemic/reperfusion; MCAO/R: middle cerebral artery occlusion/reperfusion; MCAO: middle cerebral artery occlusion; SD: Sprague Dawley; H/I: hypoxic ischemic; HBMECs: human brain microvascular endothelial cells; Bcl-2: B-cell lymphoma 2; MALAT1: Metastasis-Associated Lung Adenocarcinoma Transcript 1; bEnd.3: brain microvascular endothelial cells; OGD: oxygen-glucose deprivation; HIE: hypoxic-ischemic encephalopathy; CA/CCR: Cardiac Arrest/Cardiopulmonary Cerebral Resuscitation; GAS5: Growth Arrest-Specific 5; PUMA: p53-upregulated modulator of apoptosis; NEAT1: Nuclear paraspeckle assembly transcript 1; MIAT: myocardial Infarction Associated Transcript; PVT1: plasmacytoma variant translocation 1; HUVECs: human umbilical vein endothelial cells; ATG14: autophagy-related 14; XIAP: X chromosome-linked inhibitor of apoptosis; MEG3: Maternally expressed gene 3; DEX: dexmedetomidine; and HCN2: human cortical neurons.