Doctor Nicola Maurea

Doctor Nicola Maurea

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

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Prof. Nicola Maurea was born in Naples on 30.04.1961. In 1985 he received a degree in Medicine and Surgery from the University of Naples. In 1988 he obtained the Specialization in Cardiovascular Diseases at the University of Naples. In 1993 he obtained the Specialization in Internal Medicine at the University of Naples. In 1995 he attended the Echocardiography Laboratory of Duke University Medical Center in Boston, USA. In 1996 he attended the Echocardiography laboratory of the Thorax Center in Rotterdam, Holland. Since January 2005 he has been Director of the Division of Cardiology of the National Cancer Institute IRCCS Pascale Foundation of Naples. Since January 2008 he has been Director of the Departmental Emergency Area INT Pascale Foundation. He is the author of several international publications. His area of experience is in the field of clinical and translational cardioncology.

Presentations

Soluble guanylate cyclase activator vericiguat prevents anthracycline-mediated cardiotoxicity and sarcopenia through NO-sGC-cGMP-NLRP3 pathway

Event: Heart Failure 2024

Topic: Cardio-Oncology

Session: How to improve prognosis in cardio-oncology

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Sodium-glucose cotransporter 2 inhibitor Dapagliflozin reduces systemic H-FABP and monocyte-to-lymphocyte ratio in preclinical models of antracycline induced cardiotoxicity

Event: Heart Failure 2024

Topic: Cardio-Oncology

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

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SGLT2 i Dapagliflozin reduces NF-kB expression in heart and kydneys of preclinical models exposed to doxorubicin through MYd-88 and NLRP3 pathways: an hystological study

Event: ESC Congress 2023

Topic: Cardio-Oncology

Session: Cardiotoxicity: mechanisms, biomarkers, and treatment

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SGLT2i Dapagliflozin decreases NLRP3, IL-1 and PCSK9 expression in preclinical models of short-term doxorubicin cardiotoxicity

Event: ESC Congress 2023

Topic: Cardio-Oncology

Session: Cardiotoxicity: mechanisms, biomarkers, and treatment

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Anti CTLA-4 and PD-1 monoclonal antibodies increases systemic SDF-1 and galectin-3 levels and reduces myocardial strain through NLRP3 and MyD-88 pathways

Event: ESC Congress 2023

Topic: Cardio-Oncology

Session: T-cells, checkpoint inhibitors, and cardiac complications

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Dapagliflozin improves radial and longitudinal strain, increases pAMPK and reduces myocardial and renal NF-kB expression in preclinical models of doxorubicin cardiotoxicity through NLRP3 and Myd-88

Event: EACVI 2023

Topic: Tissue Doppler, Speckle Tracking and Strain Imaging

Session: Dechiphering the phenotypes and dynamics of cardiomyopathies under the light of multi-modality imaging

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CTLA-4 and PD-1 blocking agents affects longitudinal and radial strain in preclinical models, increases systemic SDF-1, cardiac fibronectin, S-100 calgranulin, galectine-3 and NLRP-3/MyD-88 pathways

Event: EACVI 2023

Topic: Tissue Doppler, Speckle Tracking and Strain Imaging

Session: Deformation Imaging 1

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Berberine associated to SGLT2i Dapagliflozin synergistically reduces cardiac cell apoptosis during exposure to Trastuzumab through reduction of AGEs and IL-6 and induction of pAMPK

Event: ESC Congress 2022

Topic: Cardiotoxicity of Drugs

Session: Drug cardiotoxicity: what do we need to know?

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Pembrolizumab, Ipilimumab and Nivolumab reduces cardiac pAMPK and IL-10, increases vascular NF-kB expression and levels of IL-1b, IL-2 and IL-6 in myocardial tissue

Event: ESC Congress 2022

Topic: Cardiotoxicity of Drugs

Session: Drug cardiotoxicity: what do we need to know?

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Sacubitril-valsartan activates pAMPK and reduces NLRP3, MyD88, cytokines/growth factors and DAMPs in doxorubicin-treated mice improving longitudinal strain and ejection fraction

Event: ESC Congress 2022

Topic: Cardiotoxicity of Drugs

Session: Drug cardiotoxicity: what do we need to know?

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Doctor Nicola Maurea

Biography

Contributor content

Soluble guanylate cyclase activator vericiguat prevents anthracycline-mediated cardiotoxicity and sarcopenia through NO-sGC-cGMP-NLRP3 pathway

Sodium-glucose cotransporter 2 inhibitor Dapagliflozin reduces systemic H-FABP and monocyte-to-lymphocyte ratio in preclinical models of antracycline induced cardiotoxicity

SGLT2 i Dapagliflozin reduces NF-kB expression in heart and kydneys of preclinical models exposed to doxorubicin through MYd-88 and NLRP3 pathways: an hystological study

SGLT2i Dapagliflozin decreases NLRP3, IL-1 and PCSK9 expression in preclinical models of short-term doxorubicin cardiotoxicity

Anti CTLA-4 and PD-1 monoclonal antibodies increases systemic SDF-1 and galectin-3 levels and reduces myocardial strain through NLRP3 and MyD-88 pathways

Dapagliflozin improves radial and longitudinal strain, increases pAMPK and reduces myocardial and renal NF-kB expression in preclinical models of doxorubicin cardiotoxicity through NLRP3 and Myd-88

CTLA-4 and PD-1 blocking agents affects longitudinal and radial strain in preclinical models, increases systemic SDF-1, cardiac fibronectin, S-100 calgranulin, galectine-3 and NLRP-3/MyD-88 pathways

Berberine associated to SGLT2i Dapagliflozin synergistically reduces cardiac cell apoptosis during exposure to Trastuzumab through reduction of AGEs and IL-6 and induction of pAMPK

Pembrolizumab, Ipilimumab and Nivolumab reduces cardiac pAMPK and IL-10, increases vascular NF-kB expression and levels of IL-1b, IL-2 and IL-6 in myocardial tissue

Sacubitril-valsartan activates pAMPK and reduces NLRP3, MyD88, cytokines/growth factors and DAMPs in doxorubicin-treated mice improving longitudinal strain and ejection fraction

ESC 365 is supported by

Doctor Nicola Maurea Follow

Biography

Contributor content

Soluble guanylate cyclase activator vericiguat prevents anthracycline-mediated cardiotoxicity and sarcopenia through NO-sGC-cGMP-NLRP3 pathway

Sodium-glucose cotransporter 2 inhibitor Dapagliflozin reduces systemic H-FABP and monocyte-to-lymphocyte ratio in preclinical models of antracycline induced cardiotoxicity

SGLT2 i Dapagliflozin reduces NF-kB expression in heart and kydneys of preclinical models exposed to doxorubicin through MYd-88 and NLRP3 pathways: an hystological study

SGLT2i Dapagliflozin decreases NLRP3, IL-1 and PCSK9 expression in preclinical models of short-term doxorubicin cardiotoxicity

Anti CTLA-4 and PD-1 monoclonal antibodies increases systemic SDF-1 and galectin-3 levels and reduces myocardial strain through NLRP3 and MyD-88 pathways

Dapagliflozin improves radial and longitudinal strain, increases pAMPK and reduces myocardial and renal NF-kB expression in preclinical models of doxorubicin cardiotoxicity through NLRP3 and Myd-88

CTLA-4 and PD-1 blocking agents affects longitudinal and radial strain in preclinical models, increases systemic SDF-1, cardiac fibronectin, S-100 calgranulin, galectine-3 and NLRP-3/MyD-88 pathways

Berberine associated to SGLT2i Dapagliflozin synergistically reduces cardiac cell apoptosis during exposure to Trastuzumab through reduction of AGEs and IL-6 and induction of pAMPK

Pembrolizumab, Ipilimumab and Nivolumab reduces cardiac pAMPK and IL-10, increases vascular NF-kB expression and levels of IL-1b, IL-2 and IL-6 in myocardial tissue

Sacubitril-valsartan activates pAMPK and reduces NLRP3, MyD88, cytokines/growth factors and DAMPs in doxorubicin-treated mice improving longitudinal strain and ejection fraction

ESC 365 is supported by

Doctor Nicola Maurea