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Arterial Stiffness in Chronic Obstructive Pulmonary Disease
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In: Advances in Arterial Stiffness Research ISBN: 978-1-63485-838-0
Editor: Becky Chavez © 2016 Nova Science Publishers, Inc.
Chapter 4
WNT OSTEOBLAST PATHWAY AND
OSTOPROTEGERIN: LINKS BETWEEN BONE
TURNOVER, VASCULAR CALCIFICATIONS
AND ARTERIAL STIFFNESS
Eirini Stavrinou, Charalambos Koumaras
and Aikaterini Papagianni
*
Department of Nephrology, Medical School, Aristotle University of
Thessaloniki, Hippokration Hospital, Thessaloniki, Greece
ABSTRACT
Arterial stiffness is associated with medial arterial calcifications
which are commonly observed in certain patient groups such as
elderly, diabetic and chronic kidney disease patients and is a significant
predictor of cardiovascular morbidity and mortality, independent of
well-established traditional cardiovascular risk factors. The underlying
pathogenetic mechanisms are complex and not yet clearly defined;
however, recently research has focused on the link between disordered
bone turnover and arterial calcifications and stiffness and the regulatory
factors and molecular pathways of this process. The inhibitors of the
canonical Wnt/β-catenin signaling pathway of the osteoblasts, sclerostin
and Dickkopf-1 related protein (DKK-1), exert anti-anabolic activity in
*
Corresponding Author Email: aikpapag@otenet.gr.
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Eirini Stavrinou, Charalambos Koumaras and Aikaterini Papagianni
76
bones and have been related to vascular calcifications, arterial stiffness
and adverse clinical outcomes. Osteoprotegerin, a negative regulator
of osteoclast activity via RANKL inhibition, has also been associated
with vascular calcifications and arterial stiffness. Moreover, recent
epidemiologic data indicate that the aforementioned molecules, despite
their opposing actions in bone turnover, may exhibit an additive effect on
extra-osseous bone formation. Clearly, further research is needed to
identify the exact molecular interactions between bone turnover and
arteriosclerotic vascular changes which would hopefully introduce new
therapeutic strategies against cardiovascular disease.
Keywords: arterial stiffness, cardiovascular disease, chronic kidney disease,
diabetes mellitus, Dickkopf-1, osteoporosis, osteoprotegerin, sclerostin,
vascular calcifications, Wnt osteoblast pathway
INTRODUCTION
Arterial remodeling observed with advancing age is associated with both
atherosclerotic and arteriosclerotic vascular changes which share some
common etiologic factors. Atherosclerosis is a local inflammatory disease,
affecting primary medium-sized arteries and is associated with increased
arterial intimal-media thickness, plaque formation and intimal calcification
leading to luminal obstruction and subsequently to ischemic cardiovascular
(CV) events. In contrast, arteriosclerosis is a diffuse disease, affecting mainly
large elastic and medium-sized arteries and characterized by media thickening
and calcification, resulting in progressive loss of arterial compliance and
stiffening [1, 2]. Intimal and medial calcifications may occur independently of
each other; however, particularly in certain patients groups, including diabetics
and chronic kidney disease (CKD) patients, they often coexist and follow an
accelerated course stiffness contributing to the excessive CV morbidity and
mortality rates observed in these patients populations.
Recent evidence suggests that vascular calcification is not simply a
passive process of mineral deposition but a highly regulated active process in
which the trans-differentiation of vascular smooth muscle cells (VSMCs) into
osteoblast-like cells plays a central role [3]. A variety of factors that influence
this process have been recognized, including dysregulated mineral
homeostasis and bone turnover, as well as imbalance between promoters and
inhibitors of extra-osseous bone formation [4-8]. Thus, it appears that there is
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