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Circulating cytokines/chemokines and growth factors regulate endothelial function1 and influence the development of cardiovascular diseases.2 Cardiovascular diseases are characterized by endothelial dysfunction,3 vascular smooth muscle cell (VSMC) proliferation,4 and inflammatory cell migration, leading to obliteration or excessive enlargement of vascular lumens.5 Endothelial dysfunction is induced by cardiovascular risk factors, including hypertension, diabetes mellitus, dyslipidemia, and smoking, all of which trigger a variety of vascular disorders. Recently, AMP-activated protein kinase (AMPK) has been demonstrated as an important regulator of metabolic functions, including the regulation of cellular energy homeostasis and metabolism.6 AMPK is an evolutionarily conserved serine/threonine kinase that functions as an important energy sensor and plays a crucial role in vascular homeostasis. Moreover, AMPK is a master regulator that senses cellular energetics in part through the AMP/ATP ratio and mitochondrial reactive oxygen species production and coordinates cell-autonomous responses to metabolic stress.7 Importantly, AMPK has an antiapoptotic effect in endothelial cells and a proapoptotic effect in VSMCs, which are critical for vascular remodeling.8 The interactions between endothelial cells, VSMCs, adventitial cells, and inflammatory cells play crucial roles in the development of vascular diseases. Both endothelial nitric oxide (NO) production and NO-mediated signaling in endothelial cells and VSMCs are targets and effectors of the AMPK signaling pathway.9 Furthermore, AMPK regulates many other stimuli modulating vascular functions, including reactive oxygen species, that promote VSMC proliferation by auto/paracrine growth mechanisms. AMPK is a heterotrimeric complex consisting of a catalytic subunit (α) and 2 regulatory subunits (β and γ), each having ≥2 isoforms (α1, α2, β1, β2, γ1, γ2, and γ3) that are differentially expressed …

AMPKα2 Regulates Hypoxia-Inducible Factor-1α Stability and Neutrophil Survival to Promote Vascular Repair After Ischemia