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Forum on Immunopathological Diseases and Therapeutics
SJR: 0.309 SNIP: 0.041 CiteScore™: 0.18

ISSN Imprimir: 2151-8017
ISSN On-line: 2151-8025

Archives: Volume 1, 2010 to Volume 7, 2016

Forum on Immunopathological Diseases and Therapeutics

DOI: 10.1615/ForumImmunDisTher.2013008768
pages 133-147

RAGE and NF-κB Signaling in Heart Disease

Hans Christian Volz
Department of Cardiology, Angiology and Pneumology, University Hospital of Heidelberg, Heidelberg, Germany
Stephan Schiekofer
Center of Geriatric Medicine, Bezirksklinikum Regensburg, Regensburg, Germany
Ziya Kaya
Department of Cardiology, Angiology and Pneumology, University Hospital of Heidelberg, Heidelberg, Germany
Hugo A. Katus
Department of Cardiology, Angiology and Pneumology, University Hospital of Heidelberg, Heidelberg, Germany
Martin Andrassy
Department of Cardiology, Angiology and Pneumology, University Hospital of Heidelberg, Heidelberg, Germany

RESUMO

Advanced glycation end products (AGEs), S100/calgranulins, high-mobility group box (HMGB)1-protein, amyloid β-peptides, and the family of β-sheet fibrils have been shown to contribute to a number of chronic diseases such as diabetes, amyloidosis, and cancer by promoting cellular dysfunction via binding to the receptor for advanced glycation end products (RAGE). Engagement of RAGE leads to the activation of the nuclear factor (NF)-κB superfamily of transcription factors, which have been implicated in the regulation of numerous cellular processes such as cell survival, apoptosis, and secretion of cytokines in many cell types in immune cells but also cardiomyocytes, endothelial cells, and fibroblasts. However, sustained activation of NF-κB seems to be detrimental and promotes the development of heart failure by eliciting signals that trigger chronic inflammation through enhanced elaboration of various cytokines including tumour necrosis factor a (TNF-α), interleukin-1 (IL-1), and interleukin 6 (IL-6). Furthermore, engagement of RAGE appears to lead to prolonged NF-κB-mediated activation overwhelming endogenous autoregulatory feedback inhibition loops. The underlying mechanisms that account for the multifaceted and differential effects of NF-κB on cardiac cells are presently not fully understood. In this review, we will focus on the role of RAGE as a master switch of inflammation by converting a brief pulse of cellular activation to sustained cellular dysfunction. Furthermore, we discuss how duration of activation and cellular context may explain mechanistically the differential effects of NF-κB signaling in the heart.


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