Abstract
Vascular calcification (VC) is an urgent worldwide health issue with no available medical treatment. It is an active cell-driven process by osteogenic differentiation of vascular cells with complex mechanisms. The AMP-activated protein kinase (AMPK) serves as the master sensor of cellular energy status. Accumulating evidence reveals the vital role of AMPK in VC progression. AMPK is involved in VC in various ways, including inhibiting runt-related transcription factor 2 signaling pathways, triggering autophagy, attenuating endoplasmic reticulum stress and dynamic-related protein 1-mediated mitochondrial fission, and activating endothelial nitric oxide synthase. AMPK activators, like metformin, are associated with reduced calcification deposits in certain groups of patients, indicating that AMPK is a potential therapeutic target for VC.
Highlights
Vascular calcification (VC) is characterized by accumulating calcium deposits in the tunica intima and tunica media of the vessel wall
The contractile phenotype is predisposed to osteoblastic phenotypic transition under certain local stimuli like inflammation [9]. This phenotypic transdifferentiation is a hallmark in the pathogenesis of VC, which is characterized by the loss of contraction-related proteins and the accumulation of osteoblasticinvolved proteins, including runt-related transcription factor 2 (Runx2), alkaline phosphatase (ALP), and osteopontin [9,10,11]
These findings suggest the activation of AMPK-Endothelial nitric oxide synthase (eNOS)-nitric oxide (NO) signaling pathway is associated with the amelioration of VC
Summary
Vascular calcification (VC) is characterized by accumulating calcium deposits in the tunica intima and tunica media of the vessel wall. Vascular smooth muscle cells (VSMCs) are the essential constituents of the vascular wall Those contraction-related proteins secreted by contractile type of VSMCs are critical for regulating blood pressure and maintaining the extracellular matrix (ECM) of vessels [8]. The contractile phenotype is predisposed to osteoblastic phenotypic transition under certain local stimuli like inflammation [9] This phenotypic transdifferentiation is a hallmark in the pathogenesis of VC, which is characterized by the loss of contraction-related proteins and the accumulation of osteoblasticinvolved proteins, including runt-related transcription factor 2 (Runx2), alkaline phosphatase (ALP), and osteopontin [9,10,11]. Intracellular Ca2+ can activate AMPK by phosphorylating Thr172 by calmodulin-dependent protein kinase CaMKKβ [17, 18] Both canonical and non-canonical mechanisms are involved in the Ca2+/CaMKKβ pathway. We will focus on the recent advances concerning the role of AMPK in VC and interpret its potential therapeutic utility
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