Copyright © 2006, European Society of Cardiology
Innate immunity and inflammation – New frontiers in comparative cardiovascular pathology
aDepartments of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, USA
bDiagnostic Medicine and Pathobiology, Kansas State University, Manhattan, KS 66506, USA
cHuman Nutrition, Kansas State University, Manhattan, KS 66506, USA
* Corresponding author. Email address: tmelgare{at}ksu.edu
Innate immunity and inflammation play key roles in a wide range of pathology – including heart disease and vasculopathies. Current thinking suggests "damage" rather than "foreignness" as the actual trigger of the immune system, which has caused a dramatic change in how we tend to view the etiopathology of most types of heart disease. The future potential of certain anti-inflammatory therapeutic strategies in addressing heart disease is intriguing. Still, the Janus face of immunity/inflammation cannot be over emphasized as adverse manipulation of these systems may prove ineffectual or worse, damaging. Knowledge on functional characteristics of individual immune mediators is undoubtedly a central theme, but in depth understanding of the multiple biological actions of these molecules, as well as their contextual function, is the corner stone in deciding on potential future targets for pharmacologic manipulation. Animal models of human heart disease are currently being investigated and clinical trials conducted to gain further knowledge in this essential area of cardiovascular research, but the scarcity of cardiovascular research focusing on signaling molecules and pathways of innate immunity is still evident. Genomic and proteomic research in heart disease is going through its formative years, and much is still unknown about the complex pathway dynamics utilized by the innate immune system. This review will provide an overview of the current literature focusing on innate immunity and the heart, and hopefully will spark an interest in further basic as well as clinical research. As more information on cardiovascular immunity becomes available, this will provide a better understanding and thus act as the foundation for potential development of new treatment strategies for treatment of cardiovascular disorders.
KEYWORDS Toll like receptors; Antimicrobial peptides; Nuclear factor kappa beta; Innate immunity
Time for primary review 27 days
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  R. L Kao, W. Browder, and C. Li Cellular Cardiomyoplasty: What Have We Learned? Asian Cardiovasc Thorac Ann, January 1, 2009; 17(1): 89 - 101. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Ye, Y. Lin, J. R. Perez-Polo, B. F. Uretsky, Z. Ye, B. C. Tieu, and Y. Birnbaum Phosphorylation of 5-Lipoxygenase at Ser523 by Protein Kinase A Determines Whether Pioglitazone and Atorvastatin Induce Proinflammatory Leukotriene B4 or Anti-Inflammatory 15-Epi-Lipoxin A4 Production J. Immunol., September 1, 2008; 181(5): 3515 - 3523. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Takahashi Toll-like receptors and myocardial contractile dysfunction Cardiovasc Res, April 1, 2008; 78(1): 3 - 4. [Full Text] [PDF]
|
|
|
|
|
|
P. Knuefermann, M. Schwederski, M. Velten, P. Krings, H. Ehrentraut, M. Rudiger, O. Boehm, K. Fink, U. Dreiner, C. Grohe, et al. Bacterial DNA induces myocardial inflammation and reduces cardiomyocyte contractility: role of Toll-like receptor 9 Cardiovasc Res, April 1, 2008; 78(1): 26 - 35. [Abstract] [Full Text] [PDF]
|
|