This is another window-to-the-future article that caught my eye because, really, I just wanted to see what a Frizzled signal was.
And, it turns out, it’s mildly interesting.
My area of expertise is not cell signaling and infarct-related myocardial fibroblast migration/inhibition, so the first few pages of cell plating and luciferase expression measurement are not my cup of tea. However, eventually, the authors get around to injecting UM206 into a mouse MI model and find significant reductions in infarct size, increased myofibroblasts, and, more importantly, increased ejection fraction/decreased mortality from heart failure.
Give it another five years, and maybe we’ll be giving our ACS patients aspirin, clopidogrel, and a Frizzled-antagonist.
“Blocking of Frizzled Signaling With a Homologous Peptide Fragment of Wnt3a/Wnt5a Reduces Infarct Expansion and Prevents the Development of Heart Failure After Myocardial Infarction.”
circ.ahajournals.org/content/…/CIRCULATIONAHA.110.976969.abstract