Copyright: ©Author(s) 2026.
World J Transl Med. Nov 28, 2026; 12(4): 124606
Published online Nov 28, 2026. doi: 10.5528/wjtm.124606
Published online Nov 28, 2026. doi: 10.5528/wjtm.124606
Figure 3 Schematic representation of the mechanisms of action of GalNAc-conjugated therapies targeting lipoprotein(a) gene expres sion, reducing apolipoprotein(a) synthesis and circulating lipoprotein(a) levels through messenger RNA degradation.
A: N-acetylgalacto samine-asialoglycoprotein receptor-mediated hepatocyte uptake; B: RNase H-mediated apolipoprotein(a) [apo(a)] mRNA degradation by pelacarsen; C: RNA-induced silencing complex-mediated apo(a) mRNA degradation by siRNAs; D: Translation of apo(a) mRNA into apo(a) protein. GalNAc: N-acetylgalactosamine; ASGPR: Asialoglycoprotein receptor; RISC: RNA-induced silencing complex; RNase H: Ribonuclease H; apo(a): Apolipoprotein(a).
- Citation: Feliciano LD, Freire JPC, Lopes CF, Lima PHM, Costa JMC, de Melo FF. Lipoprotein(a) in clinical practice: From genetic risk assessment to therapeutic silencing. World J Transl Med 2026; 12(4): 124606
- URL: https://www.wjgnet.com/2220-6132/full/v12/i4/124606.htm
- DOI: https://dx.doi.org/10.5528/wjtm.124606