Role of N6-methyladenosine modification in central nervous system diseases and related therapeutic agents - 29/04/23



Abstract |
N6-methyladenosine (m6A) is a ubiquitous mRNA modification in eukaryotes. m6A occurs through the action of methyltransferases, demethylases, and methylation-binding proteins. m6A methylation of RNA is associated with various neurological disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), depression, cerebral apoplexy, brain injury, epilepsy, cerebral arteriovenous malformations, and glioma. Furthermore, recent studies report that m6A-related drugs have attracted considerable concerns in the therapeutic areas of neurological disorders. Here, we mainly summarized the role of m6A modification in neurological diseases and the therapeutic potential of m6A-related drugs. The aim of this review is expected to be useful to systematically assess m6A as a new potential biomarker and develop innovative modulators of m6A for the amelioration and treatment of neurological disorders.
Le texte complet de cet article est disponible en PDF.Graphical Abstract |
Highlights |
• | m6A modification plays a pivotal role in a wide variety of neurological diseases. |
• | Selective regulation of m6A modification may help to treat various neurological diseases. |
• | Therapeutic agents have shown potential in pre-clinical setting via improving m6A methylation disfunction. |
• | Further research into agents is promising for the treatment of neurological diseases. |
Abbreviations : ACC, AD, Aβ, ADRB2, AGO1, ALKBH5, ARC, CCND1/CCND2, CD73, CDH1, CDH2, CDK2, CHK1, CL, CPSF5, CPSF6, CRY1/2, CSDS, D2R, DLL3, DSP, EMT, En1, ESCRT, FAAH, FMRP, FOXM1, FTO, G6PC, Gab1, GAP-43, GBM, GFAP, GIRK, GNAO1, GRIN1, GSCs, GSK-3β, HIVEP2, HK2, HNRNPs, HSPA7, HuR, IGF1R, IGF2, ILF3, JMJD1C, LIMK 1, LOX, LXRα, m6A, SAM, METTL3, METTL14, WTAP, MA, MA2, MAP2, MAPKK6, MBD2, mBDNF, MCAO/R, MMP-9, MSI1, MTMR3, MXI1, N2A, NA, NAC, N-CDPCB, NCOR2, NKAP, NLRP3, NMDA, NOTCH3, NP, NRF2, NRIP1, Nurr1, OGD/R, PBK, PCK1, PD, PDK1, Pitx3, PPP2CA, Prkca, PRRCA2, PSD95, PTEN, R-2HG, ROS, S6RP, SCN3A, SG, SNRPD2, oTau, SNRPG, SOCS2, SPP1, SRSF7, STZ, SYN1, TBI, TCAs, TMZ, TrkB, TYROBP, UBXN1, USP29, VM, VPA, VPS25, WT1, WTAP, YAP1
Keywords : N6-methyladenosine, Neurological diseases, RNA modification, Drug, Therapeutic
Plan
Vol 162
Article 114583- juin 2023 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
L’accès au texte intégral de cet article nécessite un abonnement.
Déjà abonné à cette revue ?