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Doctor Vincenzo Quagliariello

National Cancer Institute G.Pascale Foundation IRCCS, Naples (Italy)
Membership: ESC Professional Member
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Biography
Dr. Quagliariello Vincenzo has achieved an International PhD in Translational Medicine in 2015, studying the biochemistry and pathophysiology of cancer, with particular attention to the nanomedicine as a new tool for cancer diagnosis and therapy. From 2016 he studies the pathological characteristics of the cardiotoxicity induced by anticancer drugs, with particular reference to cardioprotection strategies through drugs or new formulations (nanotechnologies). Dr. Quagliariello specifically analyzes the inflammosome and cardiac/vascular microenvironment and their role in cardiotoxicity phenomena. Other professional interests of Dr. Quagliariello are related to nutraceuticals, endocrine disruptors exposure and the study of the main cardiovascular risk factors in cancer patients.
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Contributor content

The GLP-1 receptor agonist Semaglutide preserves cardiac function, reduces inflammation-driven cardiotoxicity with cardio-renal benefits in non-diabetic models exposed to anthracyclines and HER2 block
Presentation
The GLP-1 receptor agonist Semaglutide preserves cardiac function, reduces inflammation-driven cardiotoxicity with cardio-renal benefits in non-diabetic models exposed to anthracyclines and HER2 block
NLRP3/IL-1 and MyD-88/CCL2 pathway were reduced by inclisiran under exposure to anthracyclines and HER-2 blocking agent
Presentation
NLRP3/IL-1 and MyD-88/CCL2 pathway were reduced by inclisiran under exposure to anthracyclines and HER-2 blocking agent
GLP1-RA associated with PCSK9i as chemosensitizing method and therapy of anthracycline-induced cardiotoxicity under exposure to Ox-LDL: biochemical and preclinical evidences
Presentation
GLP1-RA associated with PCSK9i as chemosensitizing method and therapy of anthracycline-induced cardiotoxicity under exposure to Ox-LDL: biochemical and preclinical evidences
Dapagliflozin in primary prevention of cardiotoxicity induced by anthracycline-trastuzumab therapy through activation of pAMPK and inhibition of MyD88 and NLRP-3
Presentation
Dapagliflozin in primary prevention of cardiotoxicity induced by anthracycline-trastuzumab therapy through activation of pAMPK and inhibition of MyD88 and NLRP-3
Dapagliflozin in primary prevention of cardiotoxicity induced by anthracycline-trastuzumab therapy through activation of pAMPK and inhibition of MyD88 and NLRP-3
Presentation
Dapagliflozin in primary prevention of cardiotoxicity induced by anthracycline-trastuzumab therapy through activation of pAMPK and inhibition of MyD88 and NLRP-3
Semaglutide and dapagliflozin synergistically prevent cancer therapy-related cardiac dysfunction in hyperglycemic conditions
Presentation
Semaglutide and dapagliflozin synergistically prevent cancer therapy-related cardiac dysfunction in hyperglycemic conditions
Dapagliflozin prevents ejection fraction and fractional shortening reduction, reduces myocardial NF-KB expression and systemic pro-inflammatory biomarkers in models of doxorubicin cardiotoxicity
Presentation
Dapagliflozin prevents ejection fraction and fractional shortening reduction, reduces myocardial NF-KB expression and systemic pro-inflammatory biomarkers in models of doxorubicin cardiotoxicity
Fructose exacerbates anthracycline and HER-2 blocking agent mediated cardiotoxicity through NLRP3 and MyD88 mediated pathways: new roles of sweeteners in cardio-oncology
Presentation
Fructose exacerbates anthracycline and HER-2 blocking agent mediated cardiotoxicity through NLRP3 and MyD88 mediated pathways: new roles of sweeteners in cardio-oncology
Combinatorial immune checkpoint blockade increases myocardial secretion of H-FABP, NT-Pro-BNP, NLRP-3, IL-1 and IL6: clinical implications in cardio-immuno-oncology
Presentation
Combinatorial immune checkpoint blockade increases myocardial secretion of H-FABP, NT-Pro-BNP, NLRP-3, IL-1 and IL6: clinical implications in cardio-immuno-oncology
Ipilimumab, pembrolizumab and nivolumab exerts different cardiac and vascular toxicity through DAMPs fibronectin-EDA, S100/calgranulin, galectine-3 and associated NLRP3 inflammasome-chemokine pathway
Presentation
Ipilimumab, pembrolizumab and nivolumab exerts different cardiac and vascular toxicity through DAMPs fibronectin-EDA, S100/calgranulin, galectine-3 and associated NLRP3 inflammasome-chemokine pathway

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