RT Journal Article
T1 Proteomic Profile of Human Aortic Stenosis: Insights into the Degenerative Process
A1 Martín-Rojas, Tatiana
A1 Gil Dones, Félix
A1 Lopez-Almodovar, Luis
A1 Padial, Luis
A1 Vivanco Martínez, Fernando
A1 Barderas, María
AB Degenerative aortic stenosis is the most common worldwide cause of valve replacement. While it shares certain risk factors with coronary artery disease, it is not delayed or reversed by reducing exposure to risk factors (e.g., therapies that lower lipids). Therefore, it is necessary to better understand its pathophysiology for preventive measures to be taken. In this work, aortic valve samples were collected from 20 patients that underwent aortic valve replacement (55% males, mean age of 74 years) and 20 normal control valves were obtained from necropsies (40% males, mean age of 69 years). The proteome of the samples was analyzed by quantitative differential electrophoresis (2D-DIGE) and mass spectrometry, and 35 protein species were clearly increased in aortic valves, including apolipoprotein AI, alpha-1-antitrypsin, serum albumin, lumican, alfa-1-glycoprotein, vimentin, superoxide dismutase Cu–Zn, serum amyloid P-component, glutathione S-transferase-P, fatty acid-binding protein, transthyretin, and fibrinogen gamma. By contrast, 8 protein species were decreased (transgelin, haptoglobin, glutathione peroxidase 3, HSP27, and calreticulin). All of the proteins identified play a significant role in cardiovascular processes, such as fibrosis, homeostasis, and coagulation. The significant changes observed in the abundance of key cardiovascular proteins strongly suggest that they can be involved in the pathogenesis of degenerative aortic stenosis. Further studies are warranted to better understand this process before we can attempt to modulate it.
PB American Chemical Society
SN 1535-3893
YR 2012
FD 2012
LK https://hdl.handle.net/20.500.14352/94501
UL https://hdl.handle.net/20.500.14352/94501
LA eng
NO Martín-Rojas, Tatiana, et al. «Proteomic Profile of Human Aortic Stenosis: Insights into the Degenerative Process». Journal of Proteome Research, vol. 11, n.o 3, marzo de 2012, pp. 1537-50. https://doi.org/10.1021/pr2005692.
NO This work was supported by grants from the Instituto de Salud Carlos III (FISPI070537,PI080970),Fondo de Investigación Sanitaria de Castilla la Mancha (FISCAM,PI2008/08), Fondo de Investigación Sanitaria de Castilla la Mancha (FISCAM PI2008/28) and Fondos Feder-Redes Telemáticas de Investigación Cooperativa (RD06/0014/1015)
NO European Commission
NO Instituto de Salud Carlos III
NO Junta de Comunidades de Castilla-La Mancha
DS Docta Complutense
RD 30 dic 2025