Pathophysiology of Vascular Calcification

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Vascular calcification can lead to cardiovascular morbidity and mortality. The initiating factors and clinical consequences depend on the underlying disease state and location of the calcification. The pathogenesis of vascular calcification is complex and involves a transformation of vascular smooth muscle cells to an osteo/chondrocytic cell that expresses RUNX2 and produces matrix vesicles. The imbalance of promoters (such as hyperphosphatemia and hypercalcemia) and inhibitors (e.g., fetuin-A) is critical in the development of vascular calcification. The altered mineral metabolism and deficiency in inhibitors are common in patients with chronic kidney disease (CKD) and is one reason why vascular calcification is so prevalent in that population.

Original languageEnglish (US)
Pages (from-to)372-380
Number of pages9
JournalCurrent Osteoporosis Reports
Volume13
Issue number6
DOIs
StatePublished - Sep 26 2015

Fingerprint

Vascular Calcification
alpha-2-HS-Glycoprotein
Hyperphosphatemia
Hypercalcemia
Chronic Renal Insufficiency
Vascular Smooth Muscle
Smooth Muscle Myocytes
Minerals
Morbidity
Mortality
Population

Keywords

  • Calcification
  • Vascular calcification
  • Vascular smooth muscle cells

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism

Cite this

Pathophysiology of Vascular Calcification. / Chen, Xuening (Neal); Moe, Sharon.

In: Current Osteoporosis Reports, Vol. 13, No. 6, 26.09.2015, p. 372-380.

Research output: Contribution to journalArticle

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