It is now well established that hypertension is accompanied by remodeling of the arterial wall with significant modifications in extracellular matrix composition and in vascular cell phenotype. Some of these changes, particularly elastin fragments generation, increased proteases activity and activation of transforming growth factor-β signaling together with deposition of collagen and proteoglycans might generate a permissive soil for vascular calcification. On the other hand, calcium deposits within large arterial conduits can reduce vessel's elasticity and contribute to the generation of blood pressure pattern associated with vascular stiffness, namely isolated systolic hypertension. Hence, a hypothetical vicious cycle exists between hypertensive arterial damage and vascular calcification. Herein, we revised clinical and basic science findings supporting this possibility.
Department of Medicine, University of Padova, Treviso, Italy
Correspondence to Paolo Pauletto, MD, Department of Medicine, Medicina Interna I, Ospedale Ca’ Foncello, Via Ospedale, 31100 Treviso, Italy. Tel: +39 04 2232 2207; fax: +39 04 2232 2314; e-mail: firstname.lastname@example.org
Abbreviations: ACDC, arterial calcification and distal joint calcification; BP, blood pressure; CKD, chronic kidney disease; CVC, calcifying vascular cell DDR1; discoidin domain receptor-1 ECM; extracellular matrix EDP; elastin degradation product; ENPP1, ectonucleotide pyrophosphatase/phosphodiesterase 1; GACI, generalized arterial calcification of infancy; ISH, isolated systolic hypertension; LLC, large latent complex; MGP, matrix-gla protein; MMP, metalloproteinase; PP, pulse pressure; PPi, inorganic pyrophosphate; PWV, pulse wave velocity; PXE, Pseudoxanthoma elasticum; TG2, transglutaminase-2; TGFβ, transforming growth factor-β VSMC, vascular smooth muscle cell
Received 18 January, 2012
Revised 5 May, 2012
Accepted 8 June, 2012