Table 8 Epigenetic and posttranslational modification of Ferroptosis in neurological diseases
Diseases | Modification | Targets | Biological functions | Ref |
|---|---|---|---|---|
PD | ncRNA | SLC7A11 | Upregulated LncNEAT1 promotes MPP+-induced ferroptosis via regulating LncNEAT1/miR-150-5p/BAP1/SLC7A11 pathway in SK-N-SH cells. | |
PD | ncRNA | FTH1 | miR-335 promotes ferroptosis through the degrading of FTH1 in in vivo and in vitro 6-OHDA-stimulated models of PD. | |
PD | ncRNA | GPX4 | Midbrain dopamine oxidation promotes ferroptosis of dopaminergic neurons through facilating NEDD4-mediated ubiquitination of GPX4. | |
AIS | ncRNA | ACSL4 | Upregulated circular RNA Carm1 inhibit ferroptosis through binding circular RNA Carm1microRNA-3098-3p to downregulate ACSL4 in OGD/R-treated HT22 cells. | |
AIS | ncRNA | TFR1 | Upregulated LncRNA PVT1 promotes ferroptosis through downregulating miR-214-mediated TFR1 and p53. | |
AIS | ncRNA | Nrf2 | miR-27a promotes ferroptosis through inhibiting Nrf2 during ischemic stroke. | |
AIS | ncRNA | SLC7A11 | miR-27a promotes ferroptosis through to aggravate cerebral ischemia-reperfusion injury through inhibiting SLC7A11. | |
AIS | ncRNA | GPX4 | miR-760-3p in ADSC-Exo contributed to their function in inhibiting ferroptosis by targeting CHAC1 in neurons. | |
AIS | ncRNA | ATG7 | GATA6 suppresses neuronal autophagy and ferroptosis through miR-193b/ATG7 axis-dependent Mechanism. | |
AIS | ncRNA | GPX4 | LncRNA Meg3 promotes OGD hyperglycemic reperfusion-induced ferroptosis through upregulating p53, thereby inhibiting GPX4 in RBMVECs. | |
AIS | Methylation | PINK1 | ELAVL1 suppresses ferroptosis-induced cerebral I/R and subsequent brain damage through inhibiting PINK1 expression via stabilizing DNMT3B mRNA. | |
AIS | Ubiquitination | NCOA4 | USP14 stabilizes NCOA4 to promotes ferritinophagy-mediated ferroptosis in ischemic stroke. | |
AIS | Acetylation | TfR1/GPX4 | HDAC9 promotes neuronal ferroptosis through increasing HIF-1 by deacetylation and deubiquitination, thus promoting the transcription of TfR1 and reducing Sp1 protein levels by deacetylation and ubiquitination, thus resulting in a down-regulation of GPX4 in in vitro and in vivo models of stroke. | |
ICH | ncRNA | ACSL4 | LncRNA H19 protects against intracerebral hemorrhage injuries via regulating microRNA-106b-5p/ACSL4. | |
ICH | ncRNA | COX2/PGE2 | miR-137 inhibit ferroptosis in oxyHb-treated SH-SY5Y cells via COX2/PGE2 pathway. | |
ICH | ncRNA | FPN | Downregulation of miR-124 enhances FPN expression and attenuates iron accumulation. | |
ICH | ncRNA | Nrf2/GPX4 | Acupuncture may alleviate the neuronal cell death, inflammation, and ferroptosis after ICH by down-regulating miR-23a-3p. | |
TBI | ncRNA | 5-LOX | Increased circPtpn14 (mmu_circ_0000130), which sponge miR-351-5p, thereby upregulate the expression of 5-ALOX. | |
TBI | ncRNA | Ptgs2 | Decreased miR-212-5p was found in the TBI. Overexpression of miR-212-5p attenuates cell death through inhibiting ferroptosis via repressing Ptgs2. | |
SCI | ncRNA | FSP1 | miR-672-3p enhances functional recovery with contusive SCI through inhibiting ferroptosis via upregulating FSP1. | |
SCI | ncRNA | FSP1 | MSCs-exosomes lncGm36569 attenuates neuronal dysfunction through inhibiting ferroptosis via sponging miR-5627-5p to induce FSP1 upregulation. | |
SCI | ncRNA | GPX4 | Silencing miR-6315 attenuates neuronal dysfunction through inhibiting ferroptosis via upregulating GPX4. | |
SCI | Ubiquitination | HMOX-1 | Downregulated USP7 and upregulated HMOX-1 was found in SCI rat models. USP7 overexpression alleviates SCI through facilitating the expression of HMOX-1 through deubiquitination, thereby reducing ferroptosis. | |
MS | Methylation | GPX4 | The histone methyltransferase G9a promotes neurodegeneration through inducing ferroptosis via catalyzing the repressive mark H3K9me2 that suppresses the expression of GCLC, CBS, and GPX4. | |
MS | ncRNA | EZH2/SLC7A11 | BMSC-Exos containing miR-367-3p attenuates the severity of EAE through suppressing ferroptosis via restraining EZH2 expression, leading to the overexpression of SLC7A11. |
