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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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oxidised low-density lipoprotein (oxLDL) which then accumulates inside cells ( 2 ) causing interleukin-1β (IL-1β) production and release ( 3 ). Experimental studies in animal models ( 4 ) and recent trials, e.g. CANTOS ( 5 ), have indicated that the IL-1β

Article Type:
Research Article
DOI:
https://doi.org/10.1530/VB-22-0009
Volume/Issue:
Volume 4: Issue 1
Open access
Jamie I van der Vaart Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands
Einthoven Laboratory for Vascular and Regenerative Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Robin van Eenige Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands
Einthoven Laboratory for Vascular and Regenerative Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Patrick C N Rensen Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands
Einthoven Laboratory for Vascular and Regenerative Medicine, Leiden University Medical Center, Leiden, The Netherlands

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Sander Kooijman Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands
Einthoven Laboratory for Vascular and Regenerative Medicine, Leiden University Medical Center, Leiden, The Netherlands

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). As a result, immune cells, including monocytes, T-cells, and dendritic cells, are recruited into the intima ( 3 , 23 ). The secretion of proinflammatory cytokines (e.g. macrophage-colony stimulating factor; MCSF and interleukin 1 beta; IL-1β) by

Article Type:
Review Article
DOI:
https://doi.org/10.1530/VB-23-0017
Volume/Issue:
Volume 6: Issue 1
Open access
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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expression levels of TNF-α, IL-1β and IL-6 only under hyperglycemia ( 32 , 33 ). Ding and colleagues firstly explored the role of the HMGB1-TLR4 axis in triggering cardiomyocytes apoptosis by using a TLR4-mutant mouse model ( 34 , 35 ). When the hearts of

Article Type:
Mini Review
DOI:
https://doi.org/10.1530/VB-19-0013
Volume/Issue:
Volume 1: Issue 1
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Carlo Dal Lin Department of Cardiac, Thoracic and Vascular Sciences, Padua University-Hospital, Padua, Italy

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Francesco Tona Department of Cardiac, Thoracic and Vascular Sciences, Padua University-Hospital, Padua, Italy

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Elena Osto University and University Hospital Zurich, Institute of Clinical Chemistry, Zurich, Switzerland
University Hospital Zurich, Heart Center, Zurich, Switzerland
Swiss Federal Institute of Technology (ETH), Laboratory of Translational Nutrition Biology, Zurich, Switzerland

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’ or ‘classically activated’ macrophages and secrete proteolytic and inflammatory agents (such as IL-1β, TNFα, NO, and IL-6). Later on, pro-inflammatory macrophages are replaced by macrophages with an anti-inflammatory phenotype (commonly termed

Article Type:
Mini Review
DOI:
https://doi.org/10.1530/VB-19-0023
Volume/Issue:
Volume 1: Issue 1
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Linda Alex Department of Medicine (Cardiology), The Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, Bronx, New York, USA

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Nikolaos G Frangogiannis Department of Medicine (Cardiology), The Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, Bronx, New York, USA

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cardiac interstitial cells, such as fibroblasts, acquire a matrix-degrading phenotype during the early inflammatory phase of healing, producing matrix metalloproteinases in response to stimulation with IL-1β ( 54 ), whether cardiac pericytes also

Article Type:
Mini Review
DOI:
https://doi.org/10.1530/VB-19-0007
Volume/Issue:
Volume 1: Issue 1
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Hafsa Khan International Centre for Chemical and Biological Sciences (ICCBS), Pakistan

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Tahira Ghulam Aga Khan University Medical College, Pakistan

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Naseer Ahmed Institute of Basic Medical Sciences, Khyber Medical University, Pakistan

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Muhammad Rafai Babar Aga Khan University Medical College, Pakistan

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Simon DJ Calaminus Hull York Medical School, University of Hull, UK

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Muhammad Zuhair Yusuf Aga Khan University Medical College, Pakistan

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lipoxygenase pathway. This relays the production of ‘aspirin-triggered lipoxins’ (ATL) and ‘resolvins’ (ATRv) that help to counter the inflammatory profile via reducing the production of IL1β, IL6, IL8, IL17, TNF-α and reactive oxygen species (ROS) ( 22 , 23

Article Type:
Review Article
DOI:
https://doi.org/10.1530/VB-22-0010
Volume/Issue:
Volume 5: Issue 1
Open access
Max L B Grönloh Department of Medical Biochemistry, Vascular Biology Lab, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands
Leeuwenhoek Centre for Advanced Microscopy, Section Molecular Cytology at Swammerdam Institute for Life Sciences, the University of Amsterdam, Amsterdam, the Netherlands

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Merel E Tebbens Department of Medical Biochemistry, Vascular Biology Lab, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands

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Marianthi Kotsi Department of Medical Biochemistry, Vascular Biology Lab, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands

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Janine J G Arts Leeuwenhoek Centre for Advanced Microscopy, Section Molecular Cytology at Swammerdam Institute for Life Sciences, the University of Amsterdam, Amsterdam, the Netherlands
Department of Molecular Hematology, Sanquin Research, and Landsteiner Laboratory, Molecular Cell Biology Lab, Amsterdam, the Netherlands

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Jaap D van Buul Department of Medical Biochemistry, Vascular Biology Lab, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands
Leeuwenhoek Centre for Advanced Microscopy, Section Molecular Cytology at Swammerdam Institute for Life Sciences, the University of Amsterdam, Amsterdam, the Netherlands
Department of Molecular Hematology, Sanquin Research, and Landsteiner Laboratory, Molecular Cell Biology Lab, Amsterdam, the Netherlands

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. Journal of Immunology 2010 185 4846 – 4855 . ( https://doi.org/10.4049/jimmunol.0903732 ) 34 Mclaughlin F Hayes BP Horgan CMT Beesley JE Campbell CJ & Randi AM . Tumor necrosis factor (TNF)-α and interleukin (IL)-1β down

Article Type:
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https://doi.org/10.1530/VB-23-0005
Volume/Issue:
Volume 5: Issue 1
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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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histones with DNA ( 77 ). Of interest, Apabetalone was shown to prevent the upregulation of IL-1β, IL-6 and TNF-α in human endothelial cells exposed to high glucose levels as well as in aortic plaques from ApoE -/- mice ( 78 ). However, the recent

Article Type:
Mini Review
DOI:
https://doi.org/10.1530/VB-20-0001
Volume/Issue:
Volume 2: Issue 1
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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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X Qin Y Jiang Y Wang X Liu G Chen X Yue E Sun X , MiR-135b protects cardiomyocytes from infarction through restraining the NLRP3/caspase-1/IL-1β pathway . International Journal of Cardiology 2020 307 137 – 145 . ( https

Article Type:
Review Article
DOI:
https://doi.org/10.1530/VB-21-0007
Volume/Issue:
Volume 3: Issue 1
Open access