Acute myocardial infarction (AMI), is related to a diffuse active inflammation of the coronary tree associated with rupture of one of the multiple vulnerable plaques. The presence of soluble mediators of inflammation with their synergic or antagonistic actions coordinates the physiological response determining the plaque fate and the fatal event. The present study focus on the cytokines network operating in human coronary plaques of patients died from AMI and controls, pointing out that coronaries of AMI patients produce PTX3 protein twice as that of controls and express high level of PTX3 mRNA.

Pucci, S., Fisco, T., Zonetti, M., Bonanno, E., Mazzarelli, P., Mauriello, A. (2014). PTX3: A modulator of human coronary plaque vulnerability acting by macrophages type 2. INTERNATIONAL JOURNAL OF CARDIOLOGY, 176(3), 710-717 [10.1016/j.ijcard.2014.07.109].

PTX3: A modulator of human coronary plaque vulnerability acting by macrophages type 2

PUCCI, SABINA;BONANNO, ELENA;MAZZARELLI, PAOLA;MAURIELLO, ALESSANDRO
2014-10-20

Abstract

Acute myocardial infarction (AMI), is related to a diffuse active inflammation of the coronary tree associated with rupture of one of the multiple vulnerable plaques. The presence of soluble mediators of inflammation with their synergic or antagonistic actions coordinates the physiological response determining the plaque fate and the fatal event. The present study focus on the cytokines network operating in human coronary plaques of patients died from AMI and controls, pointing out that coronaries of AMI patients produce PTX3 protein twice as that of controls and express high level of PTX3 mRNA.
20-ott-2014
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore MED/03 - GENETICA MEDICA
English
Pentraxin; Acute myocardial infarction; Macrophage type 2; CXCR1 polymorphism; Th1 inflammatory infiltrate
Pucci, S., Fisco, T., Zonetti, M., Bonanno, E., Mazzarelli, P., Mauriello, A. (2014). PTX3: A modulator of human coronary plaque vulnerability acting by macrophages type 2. INTERNATIONAL JOURNAL OF CARDIOLOGY, 176(3), 710-717 [10.1016/j.ijcard.2014.07.109].
Pucci, S; Fisco, T; Zonetti, M; Bonanno, E; Mazzarelli, P; Mauriello, A
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/89589
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