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Int. J. Mol. Sci. 2017, 18(3), 652; doi:10.3390/ijms18030652

Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure

1
Lung and Placenta Research Laboratory, Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA
2
Laboratory of Obesity and Metabolism, Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA
3
Laboratory of Osteoarthritis and Inflammatory Diseases, Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA
*
Author to whom correspondence should be addressed.
Academic Editor: Francesco B. Blasi
Received: 30 January 2017 / Revised: 7 March 2017 / Accepted: 14 March 2017 / Published: 17 March 2017
(This article belongs to the Special Issue Inhaled Pollutants Modulate Respiratory and Systemic Diseases)
View Full-Text   |   Download PDF [289 KB, uploaded 23 March 2017]   |  

Abstract

Approximately 1 billion people smoke worldwide, and the burden placed on society by primary and secondhand smokers is expected to increase. Smoking is the leading risk factor for myriad health complications stemming from diverse pathogenic programs. First- and second-hand cigarette smoke contains thousands of constituents, including several carcinogens and cytotoxic chemicals that orchestrate chronic inflammatory responses and destructive remodeling events. In the current review, we outline details related to compromised pulmonary and systemic conditions related to smoke exposure. Specifically, data are discussed relative to impaired lung physiology, cancer mechanisms, maternal-fetal complications, cardiometabolic, and joint disorders in the context of smoke exposure exacerbations. As a general unifying mechanism, the receptor for advanced glycation end-products (RAGE) and its signaling axis is increasingly considered central to smoke-related pathogenesis. RAGE is a multi-ligand cell surface receptor whose expression increases following cigarette smoke exposure. RAGE signaling participates in the underpinning of inflammatory mechanisms mediated by requisite cytokines, chemokines, and remodeling enzymes. Understanding the biological contributions of RAGE during cigarette smoke-induced inflammation may provide critically important insight into the pathology of lung disease and systemic complications that combine during the demise of those exposed. View Full-Text
Keywords: receptor for advanced glycation end-products (RAGE); secondhand smoke; disease; exposure receptor for advanced glycation end-products (RAGE); secondhand smoke; disease; exposure
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Lewis, J.B.; Hirschi, K.M.; Arroyo, J.A.; Bikman, B.T.; Kooyman, D.L.; Reynolds, P.R. Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure. Int. J. Mol. Sci. 2017, 18, 652.

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