Cardiac Fibroblast GSK-3α Aggravates Ischemic Cardiac Injury by Promoting Fibrosis, Inflammation, and Impairing Angiogenesis

To determine the role of fibroblast-glycogen synthase kinase-3 (GSK-3)α in myocardial infarction-induced adverse cardiac remodeling, GSK-3α was deleted specifically in the residential fibroblast or myofibroblast using tamoxifen inducible Tcf21 or Periostin promoter-driven Cre recombinase, respectively.