Genetics of adrenergic signaling drives coronary artery calcification

TY - JOUR

T1 - Genetics of adrenergic signaling drives coronary artery calcification

AU - Gambardella, Jessica

AU - Wang, Xujun

AU - Mone, Pasquale

AU - Khondkar, Wafiq

AU - Santulli, Gaetano

N1 - Funding Information: Importantly, the influence of CAC progression by SNPs within the β2AR signal pathway was confirmed after adjustment for other risk factors, such as cholesterol levels, diabetes, systolic blood pressure, and age5. Nevertheless, the Authors did not fully delve into the potential molecular mechanisms mediated by β2AR and G proteins able to affect CAC progression. Here we propose a recent new pathway identified for β2-AR, which could be directly implicated in vessel calcification, enlightening the impact of genetic variations of this pathway in CAC progression. Indeed, recent evidence indicates that β2-AR plays a crucial role in bone-deposition; specifically, the activation of this receptor on osteoblasts, the recruitment of Gsα protein, and the increased levels of intracellular cAMP lead to osteoclastogenesis [15]. Consistent with these findings, a clinical study published in Circulation demonstrates that β2-AR signaling is implicated in aortic valve calcification [16]. Specifically, the sympatho-adrenoceptors stimulation is shown to be involved in the osteogenic differentiation of human valve cells [16]. Although not experimentally proved, it is reasonable to speculate that the participation of the β-AR signaling pathway reported in valve calcification could be translated to the CAC process. For instance, β2-AR and G protein pathways could be implicated in osteogenic differentiation of VSMCs or pericytes during artery calcification, supporting the idea that SNPs associated with this pathway are independent risk factors for CAC progression (Fig. 1).The Santulli's lab is supported in part by the NIH (R01-HL146691, R01-DK123259, R01-DK033823, and R00-DK107895 to G.S.) and by the American Heart Association (AHA-20POST35211151 to J.G.). Funding Information: The Santulli's lab is supported in part by the NIH ( R01-HL146691 , R01-DK123259 , R01-DK033823 , and R00-DK107895 to G.S.) and by the American Heart Association ( AHA-20POST35211151 to J.G.).

PY - 2020/10

Y1 - 2020/10

KW - Atherosclerosis

KW - Coronary artery calcification

KW - Vessel

KW - β2-adrenergic receptor

UR - http://www.scopus.com/inward/record.url?scp=85089915753&partnerID=8YFLogxK

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U2 - 10.1016/j.atherosclerosis.2020.07.025

DO - 10.1016/j.atherosclerosis.2020.07.025

M3 - Editorial

C2 - 32863027

AN - SCOPUS:85089915753

SN - 0021-9150

VL - 310

SP - 88

EP - 90

JO - Atherosclerosis

JF - Atherosclerosis

ER -