Chapter 93. Vascular Calcification

Towler, Dwight A.; Demer, Linda L.

doi:10.1002/9780470623992.ch93

Cited by 3 publications

(2 citation statements)

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“…Moreover, as in skeletal development – where unique biology controls matrix mineralization in membranous bone, endochondral bone, dentin, and enamel6, 7 -- mechanistic diversity exists in the pathobiology of vascular calcium deposition 2, 4, 5, 8. Five common forms of vascular calcification -- each possessing unique histoanatomic characteristics and clinical settings with overlapping yet distinct molecular mechanisms -- have been described to date4, 5, 9 (Table 1). Although we touch upon the subject, the reader is referred to other contemporary reviews for in-depth consideration of pathogenic differences2, 4, 5.…”

Section: Introductionmentioning

confidence: 99%

Inflammation and the Osteogenic Regulation of Vascular Calcification

et al. 2010

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A rterial biomineralization processes have been afflicting humans for Ն5 millennia, as realized in 2003 via the computed tomographic imaging of Ö tzi, the intriguing "ice mummy" discovered in the Tyrolean Alps. 1 Patchy abdominal atherosclerotic calcification was readily detected in the postmortem of this Ϸ40-year-old hunter of the early Copper Age, by 2000 years a predecessor of King Tutankhamen. 1 Today, an epidemic of vascular calcification is emerging within our aging and dysmetabolic populace. 2,3 Although vascular calcification was once considered only a passive process of dead and dying cells, work from laboratories worldwide has now highlighted that arterial biomineralization is an actively regulated form of calcified tissue metabolism. 4,5 Moreover, as in skeletal development -where unique biology controls matrix mineralization in membranous bone, endochondral bone, dentin, and enamel, 6,7 mechanistic diversity exists in the pathobiology of vascular calcium deposition. 2,4,5,8 Five common forms of vascular calcification, each possessing unique histoanatomic characteristics and clinical settings with overlapping yet distinct molecular mechanisms, have been described to date 4,5,9 (Table 1). Although we touch on the subject, the reader is referred to other contemporary reviews for in-depth consideration of pathogenic differences. 2,4,5 In this brief review and perspective, we recount recent data that emphasize inflammation and oxidative stress signaling as key contributors to the pathogenesis of vascular mineral deposition. 10 Furthermore, we highlight differences between the low-density lipoprotein receptor (LDLR)-deficient and apolipoprotein E (apoE)-deficient murine models ( Table 2) that help articulate the multifaceted contributions of dyslipidemia, diabetes mellitus, and uremia to arterial calcium deposition. 2,4,11 We end by summarizing the importance of considering these disease stage-and context-specific contributions arterial mineralization when crafting therapeutic strategies to address the disease burden of vascular calcification that increasingly afflicts our patients. 5 28 -32 In this section, we review this new data and also highlight distinctions between the LDLR Ϫ/Ϫ and apoE Ϫ/Ϫ murine disease models 33 ( Table 2) that provide insights into the mechanistic complexities of inflammation-dependent arterial calcium accumulation. RANKL and Atherosclerotic CalcificationReceptor Activator of Nuclear Factor B Ligand/ Osteoprotegerin Signaling and Atherosclerotic Calcification The first robust evidence for the primary contributions of inflammatory cytokine signaling to pathogenesis of vascular calcification arose from the generation and evaluation of the osteoprotegerin (OPG) Ϫ/Ϫ mouse. 34 OPG-deficient mice develop severe medial and intimal arterial calcification in conjunction with high-turnover osteoporosis driven by excessive osteoclast formation. 34 OPG was first shown to function as an antagonistic "faux receptor" of receptor activator of nuclear factor B ligand (RANKL), the TNF superfamil...

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Section: Introductionmentioning

confidence: 99%

Inflammation and the Osteogenic Regulation of Vascular Calcification

et al. 2010

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“…In addition, there is an inverse relation between marrow adiposity and its ability to produce bone cells (5). Furthermore, the calcifications within blood vessels are now shown to be the result of intravascular bone formation, complete with an intact Wnt signaling pathway (6) rather than merely calcium deposition overlying damaged endothelial tissue. Moreover, the presence of the calcium sensing receptor in endocardium and aortic endothelium (7) provides further credence to the presence of a bone-forming mechanism with the ability to calcify.…”

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Gut–Bone Interactions and Implications for the Child With Chronic Gastrointestinal Disease

Klein¹

2011

J. pediatr. gastroenterol. nutr.

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Bone is not simply a framework on which to hang viscera and connective tissue; it is also a dynamic interactive organ system with roles in immunoregulation, adipogenesis, and vascular calcification, among others. Bone is intimately affected by chronic disease, including gastrointestinal disease. The mechanisms for bone loss in conditions such as inflammatory bowel disease, celiac disease, and cystic fibrosis are discussed with regard to the role of the inflammatory response. Furthermore, we raise the issue of effects of inflammation on both intestinal and renal calcium and phosphate transport, although the ways in which these actions affect bone are not explained and require further research. The stress response, a prominent feature following burn injury, is also elucidated and its relation to gastrointestinal disease is examined. We then discuss the importance of knowing the mechanism of bone loss to determine proper prevention and treatment for the bone loss in specific gastrointestinal conditions.

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