Vascular and tissue calcification are actively regulated processes that involves several mediators and macromolecules of bone metabolism. Moreover, calcification may occur through overlapping of yet distinct molecular mechanisms. Part 1 of this review analyzed the induction of osteogenesis by the inducers of osteochondrogenic phenotype BMP and bone formation. 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. In this part 2, the second theory of vascular and soft tissue calcification is reviewed. The antagonist mechanism of calcification-associated osteogenic phenotype comprises the 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. The best understanding of both mechanism and its regulation could be relevant to idientify therapeutic targets and design new and more effective treatments of vascular and soft tissue calcification.
Palabras clave: Vascular calcification; atherosclerosis; vascular smooth muscle cells; calcium deposits.
2010-12-22 | 1,019 visitas | Evalua este artículo 0 valoraciones
Vol. 22 Núm.4. Octubre-Diciembre 2010 Pags. 79-83 Lab acta 2010; 22(4)