AKT1 and endothelial dysfunction: These mechanisms may include attenuating the phenotype of macrophages M1 and to promote the phenotype of macrophages M2 and preventing endothelial dysfunction through enhancing endothelial nitric oxide synthase (eNOS) activity and nitric oxide (NO·) production via adiponectin receptors AdipoR1/R2-AMPK (Adenosine 5′-monophosphate (AMP)-activated protein kinase)-endothelial signaling and cyclooxygenase-2 (COX-2) expression and prostaglandin I2 (PGI2) production by means of calreticulin/CD91-dependent Akt (protein kinase B) signaling [15].