AKT1 and myocardial infarction: Across diabetes, myocardial infarction, heart failure, and neuroinflammatory states, shared pathways (e.g., IL-6/STAT3, TGF-β/SMAD, PI3K/AKT, MAPK/ERK, oxidative stress) suppress neuronal excitability, promote neuron-glia-fibroblast coupling, and culminate in neurofibrotic remodeling.