Federica Ilardi
University of Naples Federico II
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Publication
Featured researches published by Federica Ilardi.
Journal of the American Heart Association | 2013
Cinzia Perrino; Gabriele Giacomo Schiattarella; Anna Sannino; Gianluigi Pironti; Maria Piera Petretta; Alessandro Cannavo; Giuseppe Gargiulo; Federica Ilardi; Fabio Magliulo; Anna Franzone; Giuseppe Carotenuto; Federica Serino; Giovanna Giuseppina Altobelli; Vincenzo Cimini; Alberto Cuocolo; Assunta Lombardi; Fernando Goglia; Ciro Indolfi; Bruno Trimarco; Giovanni Esposito
Background Uncoupling protein 3 (ucp3) is a member of the mitochondrial anion carrier superfamily of proteins uncoupling mitochondrial respiration. In this study, we investigated the effects of ucp3 genetic deletion on mitochondrial function and cell survival under low oxygen conditions in vitro and in vivo. Methods and Results To test the effects of ucp3 deletion in vitro, murine embryonic fibroblasts and adult cardiomyocytes were isolated from wild‐type (WT, n=67) and ucp3 knockout mice (ucp3−/−, n=70). To test the effects of ucp3 genetic deletion in vivo, myocardial infarction (MI) was induced by permanent coronary artery ligation in WT and ucp3−/− mice. Compared with WT, ucp3−/− murine embryonic fibroblasts and cardiomyocytes exhibited mitochondrial dysfunction and increased mitochondrial reactive oxygen species generation and apoptotic cell death under hypoxic conditions in vitro (terminal deoxynucleotidyl transferase‐dUTP nick end labeling–positive nuclei: WT hypoxia, 70.3±1.2%; ucp3−/− hypoxia, 85.3±0.9%; P<0.05). After MI, despite similar areas at risk in the 2 groups, ucp3−/− hearts demonstrated a significantly larger infarct size compared with WT (infarct area/area at risk: WT, 48.2±3.7%; ucp3−/−, 65.0±2.9%; P<0.05). Eight weeks after MI, cardiac function was significantly decreased in ucp3−/− mice compared with WT (fractional shortening: WT MI, 42.7±3.1%; ucp3−/− MI, 24.4±2.9; P<0.05), and this was associated with heightened apoptotic cell death (terminal deoxynucleotidyl transferase‐dUTP nick end labeling–positive nuclei: WT MI, 0.7±0.04%; ucp3−/− MI, 1.1±0.09%, P<0.05). Conclusions Our data indicate that ucp3 levels regulate reactive oxygen species levels and cell survival during hypoxia, modulating infarct size in the ischemic heart.
American Journal of Physiology-heart and Circulatory Physiology | 2011
Cinzia Perrino; Giuseppe Gargiulo; Gianluigi Pironti; Anna Franzone; Laura Scudiero; Mario De Laurentis; Fabio Magliulo; Federica Ilardi; Giuseppe Carotenuto; Gabriele Giacomo Schiattarella; Giovanni Esposito
Exercise adaptations result from a coordinated response of multiple organ systems, including cardiovascular, pulmonary, endocrine-metabolic, immunologic, and skeletal muscle. Among these, the cardiovascular system is the most directly affected by exercise, and it is responsible for many of the important acute changes occurring during physical training. In recent years, the development of animal models of pathological or physiological cardiac overload has allowed researchers to precisely analyze the complex cardiovascular responses to stress in genetically altered murine models of human cardiovascular disease. The intensity-controlled treadmill exercise represents a well-characterized model of physiological cardiac hypertrophy because of its ability to mimic the typical responses to exercise in humans. In this review, we describe cardiovascular adaptations to treadmill exercise in mice and the most important parameters that can be used to quantify such modifications. Moreover, we discuss how treadmill exercise can be used to perform physiological testing in mouse models of disease and to enlighten the role of specific signaling pathways on cardiac function.
Cardiovascular Research | 2015
Giovanni Esposito; Gabriele Giacomo Schiattarella; Cinzia Perrino; Fabio Cattaneo; Gianluigi Pironti; Anna Franzone; Giuseppe Gargiulo; Fabio Magliulo; Federica Serino; Giuseppe Carotenuto; Anna Sannino; Federica Ilardi; Fernando Scudiero; Linda Brevetti; Marco Oliveti; Giuseppe Giugliano; Carmine Del Giudice; Michele Ciccarelli; Giovanni Renzone; Andrea Scaloni; Nicola Zambrano; Bruno Trimarco
AIMS Coronary artery disease is the leading cause of death in western countries, and its association with lower extremity peripheral artery disease (LE-PAD) represents an independent predictor of worse outcome. However, the molecular mechanisms underlying these effects are currently unknown. METHODS AND RESULTS To investigate these processes, we used in vitro approaches and several mouse models: (i) unilateral limb ischaemia by left common femoral artery ligation [peripheral ischaemia (PI), n = 38]; (ii) myocardial infarction by permanent ligation of the left descending coronary artery (MI, n = 40); (iii) MI after 5 weeks of limb ischaemia (PI + MI, n = 44); (iv) sham operation (SHAM, n = 20). Compared with MI, PI + MI hearts were characterized by a significant increase in cardiomyocyte apoptosis, larger infarct areas, and decreased cardiac function. By using a proteomic approach, we identified a ≅ 8 kDa circulating peptide, Dermcidin (DCD), secreted by ischaemic skeletal muscles, enhancing cardiomyocytes apoptosis under hypoxic conditions and infarct size after permanent coronary artery ligation. siRNA interference experiments to reduce DCD circulating levels significantly reduced infarct size and ameliorated cardiac function after MI. CONCLUSION Our data demonstrate that chronic limb ischaemia activates detrimental pathways in the ischaemic heart through humoral mechanisms of remote organ crosstalk. Thus, DCD may represent a novel important myokine modulating cardiomyocyte survival and function.
Current Vascular Pharmacology | 2014
Cinzia Perrino; Gabriele Giacomo Schiattarella; Fabio Magliulo; Federica Ilardi; Giuseppe Carotenuto; Giuseppe Gargiulo; Federica Serino; Marco Ferrone; Fernando Scudiero; Andreina Carbone; Bruno Trimarco; Giovanni Esposito
In recent years, the development of more effective drugs has provided a better prognosis and an increase in life expectancy for patients at all-stages of cancer. On the other hand, the price for the improving effectiveness of therapies against malignant tumors is the development of severe and potentially life-threatening drug reactions. Among these, cardiac toxic effects have recently gained particular attention. The term cardiotoxicity includes many possible pathological manifestations, but the most frequent is the reduction in cardiac function, potentially leading to heart failure and death. Importantly, the development of cardiac dysfunction may occur immediately after drug administration, or after years. The purpose of this review is to discuss the clinical features of cardiotoxicity, its molecular basis and novel possible strategies to reduce the likelihood of serious cardiac complications.
Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato respiratorio, Università di Napoli, Secondo ateneo | 2015
Cinzia Perrino; Laura Scudiero; Maria Piera Petretta; Gabriele Giacomo Schiattarella; Mario De Laurentis; Federica Ilardi; Fabio Magliulo; Giuseppe Carotenuto; Giovanni Esposito
Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato respiratorio, Università di Napoli, Secondo ateneo | 2015
Federica Ilardi; Fabio Magliulo; Giuseppe Gargiulo; Gabriele Giacomo Schiattarella; Giuseppe Carotenuto; Federica Serino; Marco Ferrone; Emanuele Visco; Fernando Scudiero; Andreina Carbone; Cinzia Perrino; Bruno Trimarco; Giovanni Esposito
International Journal of Cardiology | 2014
Gabriele Giacomo Schiattarella; Fabio Magliulo; Giuseppe D'Alise; Vito Mannacio; Federica Ilardi; Bruno Trimarco; Giovanni Esposito; Plinio Cirillo
European Heart Journal | 2018
Federica Ilardi; Giuseppe Gargiulo; Gabriele Giacomo Schiattarella; Giuseppe Giugliano; Roberta Paolillo; Giovanni Menafra; E De Angelis; Anna Franzone; Eugenio Stabile; Cinzia Perrino; Plinio Cirillo; Carmine Morisco; Raffaele Izzo; Valentina Trimarco; Giovanni Esposito
American Journal of Cardiology | 2018
Federica Ilardi; Giuseppe Gargiulo; Gabriele Giacomo Schiattarella; Giuseppe Giugliano; Roberta Paolillo; Giovanni Menafra; Elena De Angelis; Laura Scudiero; Anna Franzone; Eugenio Stabile; Cinzia Perrino; Plinio Cirillo; Carmine Morisco; Raffaele Izzo; Valentina Trimarco; Giovanni Esposito
International Journal of Physical Medicine and Rehabilitation | 2011
Luigi Di Serafino; Laura Scudiero; Mario De Laurentis; Federica Ilardi; Fabio Magliulo; Giuseppe Carotenuto; Cinzia Perrino; Giovanni Esposito
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Gabriele Giacomo Schiattarella
University of Texas Southwestern Medical Center
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