%0 Journal Article
%T Wnt signaling pathways in myocardial infarction and the therapeutic effects of Wnt pathway inhibitors
%A Chun-yu Zeng
%A Wei Eric Wang
%A Wen-bin Fu
%J Archive of "Acta Pharmacologica Sinica".
%D 2019
%R 10.1038/s41401-018-0060-4
%X Wnt signaling pathways and the intervention targets of Wnt pathway inhibitors. The secretion of Wnt proteins is dependent on palmitoylation by Porcupine. Frizzled and low-density lipoprotein receptor (LRP) proteins are membrane receptors for binding Wnt proteins. In the canonical Wnt pathway, Wnt binding leads to ¦Â-catenin nuclear translocation (after dissociation from a complex with Axin, glycogen synthase kinase 3¦Â (GSK3¦Â), adenomatous polyposis coli (APC) and casein kinase 1¦Á (CK1¦Á)), causing its interaction with TCF/LEF transcription factors and gene transcription. In the Wnt/PCP pathway, Wnt binding results in RhoA/ROCK and Rac/Jnk/NFAT pathway transduction. In the Wnt/Ca2+ pathway, Wnt binding leads to phospholipase C (PLC) activation and the accumulation of intracellular Ca2+, which then leads to the activation of calmodulin-dependent kinase II (CamKII), calcineurin and protein kinase C (PKC). UM206 targets the Frizzled receptor family; pyrvinium inhibits Axin degradation; ICG-001 inhibits the interaction between ¦Â-catenin and CBP; and WNT-974, CGX-1321 and GNF-6231 are porcupine inhibitor
%K Wnt pathway inhibitors
%K myocardial infarction
%K cardiac repairing
%K therapeutic effect
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6318317/