Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/124899
COMPARTIR / EXPORTAR:
logo share SHARE logo core CORE BASE
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL | DATACITE

Invitar a revisión por pares abierta
Título

AXL receptor tyrosine kinase is increased in patients with heart failure

AutorBattle Perales, Montserrat; Recarte-Pelz, Pedro CSIC; García de Frutos, Pablo CSIC ORCID
Palabras claveAXL receptor tyrosine kinase
Heart failure
Myocardial damage
Fecha de publicación15-may-2014
EditorElsevier
CitaciónInternational Journal of Cardiology 173(3): 402-409 (2014)
ResumenBackground AXL is a membrane receptor tyrosine kinase highly expressed in the heart and has a conspicuous role in cardiovascular physiology. The role of AXL in heart failure (HF) has not been previously addressed. Methods and results AXL protein was enhanced 6-fold in myocardial biopsies of end-stage HF patients undergoing heart transplantation compared to controls from heart donors (P < 0.0001). Next, we performed a transversal study of patients with chronic HF (n = 192) and a group of controls with no HF (n = 67). sAXL and BNP circulating levels were quantified and clinical and demographic data were collected. sAXL levels in serum were higher in HF (86.3 ± 2.0 ng/mL) than in controls (67.8 ± 2.0 ng/mL; P < 0.0001). Also, sAXL correlated with several parameters associated with worse prognosis in HF. Linear regression analysis indicated that serum creatinine, systolic blood pressure and atrial fibrillation, but not BNP levels, were predictive of sAXL levels. Cox regression analysis indicated that high sAXL values at enrollment time were related to the major HF events (all-cause mortality, heart transplantation and HF hospitalizations) at one year follow-up (P < 0.001), adding predictive value to high BNP levels. Conclusions Myocardial expression and serum concentration of AXL is elevated in HF patients compared to controls. Furthermore, peripheral sAXL correlates with parameters associated with the progression of HF and with HF events at short term follow-up. All together these results suggest that sAXL could belong to a new molecular pathway involved in myocardial damage in HF, independent from BNP. © 2014 Elsevier Ireland Ltd.
DescripciónMontserrat Batlle et al.
Versión del editorhttp://dx.doi.org/10.1016/j.ijcard.2014.03.016
URIhttp://hdl.handle.net/10261/124899
DOI10.1016/j.ijcard.2014.03.016
Identificadoresdoi: 10.1016/j.ijcard.2014.03.016
issn: 1874-1754
Aparece en las colecciones: (IIBB) Artículos




Ficheros en este ítem:
Fichero Descripción Tamaño Formato
Batlle-IJC-2014-v173-p402.pdf283,13 kBAdobe PDFVista previa
Visualizar/Abrir
Mostrar el registro completo

CORE Recommender

PubMed Central
Citations

27
checked on 27-mar-2024

SCOPUSTM   
Citations

45
checked on 15-abr-2024

WEB OF SCIENCETM
Citations

42
checked on 29-feb-2024

Page view(s)

531
checked on 19-abr-2024

Download(s)

556
checked on 19-abr-2024

Google ScholarTM

Check

Altmetric

Altmetric


Artículos relacionados:


NOTA: Los ítems de Digital.CSIC están protegidos por copyright, con todos los derechos reservados, a menos que se indique lo contrario.