Table 2.
Epigenetic regulatory mechanisms of KMT and KDM isoforms in ischemic stroke.
| Target | Study Model | Pathophysiological Mechanism | Regulatory Axis | Key Finding | References |
|---|---|---|---|---|---|
| G9a, SUV39H1 | PTS Induced Mice |
Apoptosis | G9a, SUV39H1/BDNF | Inhibition of G9a and SUV39H1 post-stroke promotes BDNF transcriptional activation. | [34] |
| EZH2 | MCAO/R Induced Rats |
Angiogenesis | EZH2/BDNF | EZH2 inhibition promotes BDNF transcriptional activation. | [35] |
| EZH2 | MCAO/R Induced Rats |
Apoptosis | EZH2/PI3K/Akt/mTOR | EZH2 inhibition reduces ischemia-induced apoptosis. | [37] |
| EZH2 | MCAO/R Induced Rats |
Proteostasis Disruption |
EZH2/Foxc1/Ubqln1 | Deacetylation of EZH2 promotes Foxc1 expression, subsequently upregulating Ubqln1 and reducing post-stroke protein damage. | [38] |
| SMYD2 | MCAO/R Induced Mice |
BBB Integrity | SMYD2/Sphk/S1PR | SMYD2 inhibition ameliorates blood-brain barrier damage after stroke. | [39] |
| SETD1B | MCAO/R Induced Mice |
Ferroptosis | SETD1B/Tfrc | SETD1B inhibition reduces Tfrc expression and alleviates ferroptosis. | [42] |
| KDM4A | MCAO/R Induced Rats |
Inflammation | KDM4A/NF-κB | KDM4A inhibition suppresses NF-κB activation and attenuates neuroinflammation. | [48] |
| KDM4A | MCAO/R Induced Mice |
Inflammation | KDM4A/MDM2/CTRP3 | KDM4A inhibition promotes microglial polarization toward an anti-inflammatory phenotype. | [49] |
| KDM6A | MCAO/R Induced Mice |
Inflammation | KDM6A/IRF5 | KDM6A inhibition suppresses IRF5 activation and alleviates neuroinflammation. | [51] |
| KDM6B | MCAO/R Induced Rats |
Apoptosis | KDM6B/BMP2/Bmf | KDM6B inhibition reduces post-stroke apoptosis via Bmf downregulation. | [53] |
| KDM1A | MCAO/R Induced Mice |
Apoptosis | KDM1A/SPHK2 | KDM1A inhibition reduces stroke-induced apoptosis. | [44] |
| KDM2A | MCAO/R Induced Rats |
Apoptosis | KDM2A/β-catenin | KDM2A inhibition stabilizes β-catenin protein and suppresses apoptosis. | [46] |