The pathogenesis of vascular and soft tissue calcification has been commonly associated with a passive calcium phosphate deposition. This pathology is frequently observed in patients with end-stage renal disease, diabetes, aging and osteoporosis; it can also lead to cardiovascular diseases and even sudden death. Until recently, vascular calcification was considered a non-specific response to tissue injury or necrosis; now, it is becoming increasingly clear that vascular calcification is an actively regulated process that resembles bone metabolism and involves alkaline phosphatase and other bone related proteins. Calcification may occur through overlapping of yet distinct molecular mechanisms. The first theory is the induction of osteogenesis by the inducers of osteochondrogenic phenotype BMP and bone formation. BMP2 and BMP4 have been most frequently associated with calcificant arteriolopathy. Once the osteogenic phenotype is induced, cells gain a distinctive molecular fingerprint, marked by the transcription factors, including core binding factor a (Cbfa1), Msx2, and osterix. Alternatively, the second theory is that loss of inhibitors of mineralization, such as inorganic pyrophosphate, osteopontin, bone matrix protein 7, fetuin-A, matrix y-carboxyglutamic acid Gla protein, osteoprotegerin, and smad 6, which also contribute to vascular calcification. Through a greater understanding of both mechanism and clinical consequences of vascular calcification, future therapeutic strategies may be more effectively designed and applied.
Vol. 22 Núm.3. Julio-Septiembre 2010 Pags. 56-61 Lab acta 2010; 22(3)