Doctor Vincenzo Quagliariello

Doctor Vincenzo Quagliariello

National Cancer Institute G.Pascale Foundation IRCCS, Naples (Italy)

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.

Presentations Articles

Dapagliflozin in primary prevention of cardiotoxicity induced by anthracycline-trastuzumab therapy through activation of pAMPK and inhibition of MyD88 and NLRP-3

Event: ESC Cardio-Oncology 2025

Topic: Cardio-Oncology

Session: Insights into anthracycline-induced cardiotoxicity and treatment perspectives

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GLP1-RA associated with PCSK9i as chemosensitizing method and therapy of anthracycline-induced cardiotoxicity under exposure to Ox-LDL: biochemical and preclinical evidences

Event: ESC Cardio-Oncology 2025

Topic: Cardio-Oncology

Session: Basic and translational cardio-oncology beyond anthracyclines

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Dapagliflozin in primary prevention of cardiotoxicity induced by anthracycline-trastuzumab therapy through activation of pAMPK and inhibition of MyD88 and NLRP-3

Event: Heart Failure 2025

Topic: Cardio-Oncology

Session: Young Investigator Award (YIA) Basic Science

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Semaglutide and dapagliflozin synergistically prevent cancer therapy-related cardiac dysfunction in hyperglycemic conditions

Event: ESC Preventive Cardiology 2025

Topic: Cardio-Oncology

Session: Cardiovascular protection in patients with cancer

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Dapagliflozin prevents ejection fraction and fractional shortening reduction, reduces myocardial NF-KB expression and systemic pro-inflammatory biomarkers in models of doxorubicin cardiotoxicity

Event: EuroEcho-Imaging 2024

Topic: Myocardial Disease

Session: Poster session 1

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Fructose exacerbates anthracycline and HER-2 blocking agent mediated cardiotoxicity through NLRP3 and MyD88 mediated pathways: new roles of sweeteners in cardio-oncology

Event: Heart Failure 2024

Topic: Cardio-Oncology

Session: Cardiovascular disease in special populations - cardio-oncology (1)

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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

Event: Heart Failure 2024

Topic: Cardio-Oncology

Session: Young Investigator Award (YIA) Basic Science

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Ipilimumab, pembrolizumab and nivolumab exerts different cardiac and vascular toxicity through DAMPs fibronectin-EDA, S100/calgranulin, galectine-3 and associated NLRP3 inflammasome-chemokine pathway

Event: Heart Failure 2022

Topic: Cardio-Oncology

Session: Heart Failure ePosters - focus on Comorbidities and special population

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Dapagliflozin enhanced the anticancer effects of the CTLA-4 blocking agent ipilimumab reducing its cardiotoxicity through galectine-3, Trimethylamine N-oxide (TMAO) and NLRP-3

Event: Heart Failure 2022

Topic: Cardio-Oncology

Session: Heart Failure ePosters - focus on Comorbidities and special population

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Fructosilation products and low doses of advanced glycation end-products promotes premature cell death of cardiac cells exposed to doxorubicin via activation of NLRP3, MyD88 and p53 downregulation

Event: Heart Failure 2022

Topic: Cardio-Oncology

Session: Heart Failure ePosters - focus on Comorbidities and special population

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Doctor Vincenzo Quagliariello

Biography

Contributor content

Dapagliflozin in primary prevention of cardiotoxicity induced by anthracycline-trastuzumab therapy through activation of pAMPK and inhibition of MyD88 and NLRP-3

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

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

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

Ipilimumab, pembrolizumab and nivolumab exerts different cardiac and vascular toxicity through DAMPs fibronectin-EDA, S100/calgranulin, galectine-3 and associated NLRP3 inflammasome-chemokine pathway

Dapagliflozin enhanced the anticancer effects of the CTLA-4 blocking agent ipilimumab reducing its cardiotoxicity through galectine-3, Trimethylamine N-oxide (TMAO) and NLRP-3

Fructosilation products and low doses of advanced glycation end-products promotes premature cell death of cardiac cells exposed to doxorubicin via activation of NLRP3, MyD88 and p53 downregulation

ESC 365 is supported by

Doctor Vincenzo Quagliariello Follow

Biography

Contributor content

Dapagliflozin in primary prevention of cardiotoxicity induced by anthracycline-trastuzumab therapy through activation of pAMPK and inhibition of MyD88 and NLRP-3

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

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

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

Ipilimumab, pembrolizumab and nivolumab exerts different cardiac and vascular toxicity through DAMPs fibronectin-EDA, S100/calgranulin, galectine-3 and associated NLRP3 inflammasome-chemokine pathway

Dapagliflozin enhanced the anticancer effects of the CTLA-4 blocking agent ipilimumab reducing its cardiotoxicity through galectine-3, Trimethylamine N-oxide (TMAO) and NLRP-3

Fructosilation products and low doses of advanced glycation end-products promotes premature cell death of cardiac cells exposed to doxorubicin via activation of NLRP3, MyD88 and p53 downregulation

ESC 365 is supported by

Doctor Vincenzo Quagliariello