Mediators of Inflammation

Danger Signals in Cardiovascular Disease


Publishing date
21 Feb 2014
Status
Published
Submission deadline
04 Oct 2013

Lead Editor

1Laboratory of Experimental Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands

2Kennedy Institute of Rheumatology, Nuffield Department of Orthopedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, London, UK

3Department of Internal Medicine I, University Hospital Würzburg, Comprehensive Heart Failure Center, University of Würzburg, Würzburg, Germany


Danger Signals in Cardiovascular Disease

Description

Cardiovascular disease is the leading cause of mortality and morbidity in Western societies and imposes an ever-growing socioeconomic burden to healthcare systems. Whether it is the rupture of a vulnerable atherosclerotic plaque or adverse myocardial remodeling after ischemic injury, inflammation is one of the key mediators of cardiovascular complications. In the absence of pathogens, the activation of innate or adaptive immunity in cardiovascular disease is intriguing. Endogenous signals released after tissue injury, also referred to as Damage/Danger Associated Molecular Patterns (DAMPs), may activate the same receptors involved in pathogen recognition. Matricellular proteins, oxidized lipid particles, and cytoskeletal proteins are a few examples of DAMPs that trigger inflammation. Elucidating the interaction between DAMPs and both innate and adaptive immunity can help us to dissect the complex inflammatory cascade in cardiovascular disease. A better understanding of the inflammatory response may result in improved therapeutic strategies, since previous anti-inflammatory agents were not successful or even detrimental in patients.

We invite authors to submit review and/or original research articles that seek to define the role of DAMPs in innate and/or adaptive immunity after cardiovascular injury. Research areas may involve ischemic heart disease, heart failure, atherosclerosis, or other research fields associated with cardiovascular disease (e.g., rheumatoid arthritis, cardiotoxic agents). Articles that are particularly of interest include, but are not limited to, those using human subjects and animal models for cardiovascular disease. In vitro experiments studying endogenous molecules that trigger inflammation are also welcome. Potential topics include, but are not limited to:

  • Toll-like receptor, NOD-like receptor, and receptor for advanced glycation end products (RAGE) activation and signaling in cardiovascular disease
  • The interaction between the extracellular matrix and inflammatory cells
  • Cardiovascular imaging of inflammation
  • Novel in vivo and in vitro models describing the role of DAMPs in cardiovascular inflammation and atherosclerosis
  • Novel anti-inflammatory therapeutic strategies in cardiovascular disease
  • Novel therapeutic or diagnostic targets within innate or adaptive immunity for cardiovascular disease
  • The association between DAMPs and cell death (apoptosis, necroptosis, necrosis, and autophagy)

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/mi/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/mi/dang/ according to the following timetable:


Articles

  • Special Issue
  • - Volume 2014
  • - Article ID 395278
  • - Editorial

Danger Signals in Cardiovascular Disease

Stefan Frantz | Claudia Monaco | Fatih Arslan
  • Special Issue
  • - Volume 2014
  • - Article ID 905463
  • - Research Article

Increased Expression of Chitinase 3-Like 1 in Aorta of Patients with Atherosclerosis and Suppression of Atherosclerosis in Apolipoprotein E-Knockout Mice by Chitinase 3-Like 1 Gene Silencing

Zushun Gong | Shanshan Xing | ... | Qichong Xing
  • Special Issue
  • - Volume 2013
  • - Article ID 716902
  • - Clinical Study

Complement C3c as a Biomarker in Heart Failure

A. Frey | G. Ertl | ... | S. Frantz
  • Special Issue
  • - Volume 2013
  • - Article ID 828354
  • - Review Article

S100A8 and S100A9: DAMPs at the Crossroads between Innate Immunity, Traditional Risk Factors, and Cardiovascular Disease

Alexandru Schiopu | Ovidiu S. Cotoi
  • Special Issue
  • - Volume 2013
  • - Article ID 181020
  • - Review Article

Mesenchymal Stem Cell Therapy for Cardiac Inflammation: Immunomodulatory Properties and the Influence of Toll-Like Receptors

F. van den Akker | S. C. A. de Jager | J. P. G. Sluijter
  • Special Issue
  • - Volume 2013
  • - Article ID 260464
  • - Research Article

Berberine Protects against Palmitate-Induced Endothelial Dysfunction: Involvements of Upregulation of AMPK and eNOS and Downregulation of NOX4

Ming Zhang | Chun-Mei Wang | ... | Li Chen
  • Special Issue
  • - Volume 2013
  • - Article ID 206039
  • - Review Article

Danger Signals in the Initiation of the Inflammatory Response after Myocardial Infarction

J. J. de Haan | M. B. Smeets | ... | F. Arslan
  • Special Issue
  • - Volume 2013
  • - Article ID 261054
  • - Research Article

Actin Is a Target of T-Cell Reactivity in Patients with Advanced Carotid Atherosclerotic Plaques

Elisabetta Profumo | Brigitta Buttari | ... | Rachele Riganò
  • Special Issue
  • - Volume 2013
  • - Article ID 390890
  • - Research Article

Natural Antioxidant-Isoliquiritigenin Ameliorates Contractile Dysfunction of Hypoxic Cardiomyocytes via AMPK Signaling Pathway

Xiaoyu Zhang | Ping Zhu | ... | Ji Li
  • Special Issue
  • - Volume 2013
  • - Article ID 370715
  • - Review Article

Update on the Pathophysiological Activities of the Cardiac Molecule Cardiotrophin-1 in Obesity

Mohamed Asrih | François Mach | ... | Fabrizio Montecucco
Mediators of Inflammation
 Journal metrics
Acceptance rate36%
Submission to final decision53 days
Acceptance to publication29 days
CiteScore6.000
Impact Factor3.758
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