Search

Your search keyword '"Penna, Claudia"' showing total 16 results
Start Over Author "Penna, Claudia" Publisher mdpi ag
16 results on '"Penna, Claudia"'

1. Enhancing Heart Transplantation: Utilizing Gas-Loaded Nanocarriers to Mitigate Cold/Hypoxia Stress

Author

Rubeo, Chiara, primary, Hoti, Gjylije, additional, Giordano, Magalì, additional, Molinar, Chiara, additional, Aragno, Manuela, additional, Mantuano, Beatrice, additional, Comità, Stefano, additional, Femminò, Saveria, additional, Cavalli, Roberta, additional, Trotta, Francesco, additional, Penna, Claudia, additional, and Pagliaro, Pasquale, additional

Published
2024
Full Text
View/download PDF

8. Percutaneous Coronary Intervention (PCI) Reprograms Circulating Extracellular Vesicles from ACS Patients Impairing Their Cardio-Protective Properties

Author

Femminò, Saveria, primary, D’Ascenzo, Fabrizio, additional, Ravera, Francesco, additional, Comità, Stefano, additional, Angelini, Filippo, additional, Caccioppo, Andrea, additional, Franchin, Luca, additional, Grosso, Alberto, additional, Thairi, Cecilia, additional, Venturelli, Emilio, additional, Cavallari, Claudia, additional, Penna, Claudia, additional, De Ferrari, Gaetano Maria, additional, Camussi, Giovanni, additional, Pagliaro, Pasquale, additional, and Brizzi, Maria Felice, additional

Published
2021
Full Text
View/download PDF

9. Cyclic Nigerosyl-Nigerose as Oxygen Nanocarrier to Protect Cellular Models from Hypoxia/Reoxygenation Injury: Implications from an In Vitro Model

Author

Penna, Claudia, primary, Femminò, Saveria, additional, Caldera, Fabrizio, additional, Rubin Pedrazzo, Alberto, additional, Cecone, Claudio, additional, Alfì, Edoardo, additional, Comità, Stefano, additional, Higashiyama, Takanobu, additional, Trotta, Francesco, additional, Pagliaro, Pasquale, additional, and Cavalli, Roberta, additional

Published
2021
Full Text
View/download PDF

11. The Inflammatory Cytokine IL-3 Hampers Cardioprotection Mediated by Endothelial Cell-Derived Extracellular Vesicles Possibly via Their Protein Cargo

Author

Penna, Claudia, primary, Femminò, Saveria, additional, Tapparo, Marta, additional, Lopatina, Tatiana, additional, Fladmark, Kari Espolin, additional, Ravera, Francesco, additional, Comità, Stefano, additional, Alloatti, Giuseppe, additional, Giusti, Ilaria, additional, Dolo, Vincenza, additional, Camussi, Giovanni, additional, Pagliaro, Pasquale, additional, and Brizzi, Maria Felice, additional

Published
2020
Full Text
View/download PDF

13. Redox Imbalances in Ageing and Metabolic Alterations: Implications in Cancer and Cardiac Diseases. An Overview from the Working Group of Cardiotoxicity and Cardioprotection of the Italian Society of Cardiology (SIC)

Author

Mercurio, Valentina, primary, Cuomo, Alessandra, additional, Cadeddu Dessalvi, Christian, additional, Deidda, Martino, additional, Di Lisi, Daniela, additional, Novo, Giuseppina, additional, Manganaro, Roberta, additional, Zito, Concetta, additional, Santoro, Ciro, additional, Ameri, Pietro, additional, Spallarossa, Paolo, additional, Arboscello, Eleonora, additional, Tocchetti, Carlo Gabriele, additional, and Penna, Claudia, additional

Published
2020
Full Text
View/download PDF

16. Inhibitors of NLRP3 Inflammasome in Ischemic Heart Disease: Focus on Functional and Redox Aspects.

Author

Pagliaro P and Penna C

Abstract

Myocardial ischemia-reperfusion injury (MIRI) is caused by several mechanisms, including the production of reactive oxygen species (ROS), altered cellular osmolarity, and inflammatory response. Calcium overload, altered oxygen levels, and mitochondrial ROS are also involved in these MIRI processes, resulting in the irreversible opening of the mitochondrial permeability transition pore (mPTP). These mechanisms and processes are associated with NLRP3 inflammasome priming and activation, which can also induce cell death by pyroptosis through the up-regulation of the caspase-1 pathway and IL-18 release. In addition, endothelial dysfunction, both in the presence and absence of MIRI, is also accompanied by altered oxygen levels, decreased nitric oxide production, and ROS overproduction, resulting in the expression of adhesion molecules and leukocyte infiltration in which the NLRP3 inflammasome plays a central role, thus contributing, through endothelial dysfunction, to the alteration of coronary flow, typical of ischemic heart disease. Given the intricate interrelationship between ROS and NLRP3, ROS inhibitors can reduce NLRP3 inflammasome activation, while NLRP3 inhibitors can reduce oxidative stress and inflammation. NLRP3 inhibitors have been intensively studied as anti-inflammatory agents in basic cardiovascular sciences. In this review, we analyze the interrelation between ROS and NLRP3 in ischemic heart disease and the effects of some NLRP3 inhibitors as possible therapeutic agents in this disease condition. All compounds considered in this review need larger studies to confirm their appropriate use in clinical scenarios as anti-ischemic drugs.

Published
2023
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results