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: