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Majid Almansouri Department of Infection Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK

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Pooja Patel Department of Infection Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK

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Janet Chamberlain Department of Infection Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK

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Sheila Francis Department of Infection Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK
Healthy Lifespan Institute HELSI, University of Sheffield, Medical School, Sheffield, UK

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-1β by caspase-1 ( 9 ). Active IL-1β can then be associated with the NLRP3 inflammasome ( 10 ). Only active IL-1β is released from cells and there is a myriad of mechanisms proposed, mainly in monocytic cells, including through microvesicles

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Eleonora Foglio Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy

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Laura Pellegrini Institute of Oncology Research (IOR), Bellinzona
Universita’ della Svizzera Italiana, Lugano, Switzerland

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Antonia Germani Laboratory of Vascular Pathology, Istituto Dermopatico dell’Immacolata, IDI-IRCCS, Fondazione Luigi Maria Monti, Rome, Italy

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Matteo Antonio Russo IRCCS San Raffaele Pisana, San Raffaele Open University, Rome, Italy
MEBIC Consortium, San Raffaele Open University, Rome, Italy

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Federica Limana Laboratory of Cellular and Molecular Pathology, IRCCS San Raffaele Pisana, Rome, Italy
San Raffaele Open University, Rome, Italy

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trafficking during autophagy and the attenuation of the apoptotic response through prevention of caspases activation. Finally, extracellular HMGB1 regulates the crosstalk autophagy/apoptosis by binding to the Receptor for Advanced Glycation End products (RAGE

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Isabelle Coornaert Laboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium
Infla-Med Centre of Excellence, University of Antwerp, Antwerp, Belgium

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Annelies Breynaert NatuRAPT Research Group, University of Antwerp, Antwerp, Belgium

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Nina Hermans NatuRAPT Research Group, University of Antwerp, Antwerp, Belgium

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Guido R Y De Meyer Laboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium
Infla-Med Centre of Excellence, University of Antwerp, Antwerp, Belgium

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Wim Martinet Laboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium
Infla-Med Centre of Excellence, University of Antwerp, Antwerp, Belgium

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± 2 10 ± 4 VSMCs (%) 6 ± 2 7 ± 2 0.6 ± 0.2 0.5 ± 0.2 Fibrous cap (µm) 4.4 ± 1.0 3.1 ± 0.5 2.1 ± 0.6 2.5 ± 0.6 Cleaved caspase-3 (%) 0.6 ± 0.3 1.0 ± 0.3 4 ± 3 2 ± 1 Independent samples t -test

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Manisha S Patil Heart Research Institute, Sydney, Australia
Faculty of Medicine and Health, University of Sydney, Sydney, Australia

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Siân P Cartland Heart Research Institute, Sydney, Australia
Faculty of Medicine and Health, University of Sydney, Sydney, Australia

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Mary M Kavurma Heart Research Institute, Sydney, Australia
Faculty of Medicine and Health, University of Sydney, Sydney, Australia

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endothelial cell line, hCMEC/D3 ( 63 ). Instead, in these cells, TRAIL stimulated caspase-1 activity and cell death ( 60 , 63 ). These discrepancies may reflect receptor expression, cell type, origin, or differences in the in vitro angiogenic assay methods

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Isabelle Coornaert Laboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium
Infla-Med Centre of Excellence, University of Antwerp, Antwerp, Belgium

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Annelies Breynaert NatuRAPT Research Group, University of Antwerp, Antwerp, Belgium

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Nina Hermans NatuRAPT Research Group, University of Antwerp, Antwerp, Belgium

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Guido R Y De Meyer Laboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium
Infla-Med Centre of Excellence, University of Antwerp, Antwerp, Belgium

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Wim Martinet Laboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium
Infla-Med Centre of Excellence, University of Antwerp, Antwerp, Belgium

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collagen (%) 23 ± 3 25 ± 3  ICAM-1-positive ECs (%) 81 ± 4 94 ± 4 b  VCAM-1-positive ECs (%) 44 ± 7 58 ± 10  Cleaved caspase 3 (%) 0.10 ± 0.03 0.03 ± 0.01 a Independent samples t -test. a P < 0.05, b P

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Sara Sileno Istituto Dermopatico dell’Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy

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Sara Beji Istituto Dermopatico dell’Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy

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Marco D’Agostino Istituto Dermopatico dell’Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy

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Alessandra Carassiti Istituto Dermopatico dell’Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy

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Guido Melillo Unit of Cardiology, IDI-IRCCS, Via Monti di Creta, Rome, Italy

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Alessandra Magenta Institute of Translational Pharmacology (IFT), National Research Council of Italy (CNR), Via Fosso del Cavaliere, Rome, Italy

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associated with both PASI improvement and local inflammatory response decrease ( 36 ). Interestingly, in MI, miR-135b is downregulated, and its overexpression attenuates pyroptosis, a caspase-1-dependent proinflammatory programmed cell death. Thus, miR-135b

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Dwitiya Sawant Center for Cardiovascular Research and The Heart Center, Nationwide Children’s Hospital, Columbus, Ohio, USA

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Brenda Lilly Center for Cardiovascular Research and The Heart Center, Nationwide Children’s Hospital, Columbus, Ohio, USA
Department of Pediatrics, The Ohio State University, Columbus, Ohio, USA

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Introduction miRNAs are a group of small (~22 nucleotides in length) ncRNA molecules that functionally fine tune gene expression through post-transcriptional regulation ( 1 ). Since their discovery in the nematode Caenorhabditiselegans in

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Xusheng Zhang Department of Cardiology, The First Central Clinical College of Tianjin Medical University, Tianjin, China
Department of Cardiology, Tianjin First Central Hospital, Tianjin, China
Department of Cardiology, Longgang People’s Hospital of Shenzhen, Shenzhen, Guangdong, China

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Zhanjun Huang Department of Cardiology, Longgang People’s Hospital of Shenzhen, Shenzhen, Guangdong, China

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Xiaorong Fan Department of Cardiology, Longgang People’s Hospital of Shenzhen, Shenzhen, Guangdong, China

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Xiaoqing Tan Department of Cardiology, Longgang People’s Hospital of Shenzhen, Shenzhen, Guangdong, China

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Chengzhi Lu Department of Cardiology, The First Central Clinical College of Tianjin Medical University, Tianjin, China
Department of Cardiology, Tianjin First Central Hospital, Tianjin, China

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Jianshe Yang Department of Nuclear Medicine, Shanghai Tenth People’s Hospital, Tongji University, Shanghai, China

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Introduction Vascular calcification is a common condition noted in aging, atherosclerosis, hypertension, diabetes, dyslipidemia, valvular heart disease, and chronic kidney disease ( 1 , 2 ). It is caused by heterotopic deposition of

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Sarah Costantino Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland

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Shafeeq A Mohammed Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland

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Samuele Ambrosini Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland

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Francesco Paneni Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland
University Heart Center, Cardiology, University Hospital Zurich, Zürich, Switzerland
Department of Research and Education, University Hospital Zurich, Zürich, Switzerland

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impaired glucose tolerance and 592 million people will have diabetes worldwide ( 1 ). A recent study analysing data from 6,264,226 adults (18 years of age or older) who participated in the Behavioral Risk Factor Surveillance System Survey (1993–1994 and

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Marie Mclaughlin School of Applied Sciences, Edinburgh Napier University, Edinburgh, UK

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Geraint Florida-James School of Applied Sciences, Edinburgh Napier University, Edinburgh, UK

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Mark Ross School of Applied Sciences, Edinburgh Napier University, Edinburgh, UK

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will be outlined with respect to attenuating chemotherapy-induced cardiovascular toxicity. Figure 1 Mechanisms of chemotherapy-induced apoptosis via activation of caspase cascade. ROS, reactive oxygen species. The detrimental effects of

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