Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure
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 th...
Main Authors: | , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
MDPI AG
2017-03-01
|
Series: | International Journal of Molecular Sciences |
Subjects: | |
Online Access: | http://www.mdpi.com/1422-0067/18/3/652 |
id |
doaj-f03a39ac4269475ea37a10677a9b80b9 |
---|---|
record_format |
Article |
spelling |
doaj-f03a39ac4269475ea37a10677a9b80b92020-11-24T21:54:01ZengMDPI AGInternational Journal of Molecular Sciences1422-00672017-03-0118365210.3390/ijms18030652ijms18030652Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke ExposureJoshua B. Lewis0Kelsey M. Hirschi1Juan A. Arroyo2Benjamin T. Bikman3David L. Kooyman4Paul R. Reynolds5Lung and Placenta Research Laboratory, Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USALung and Placenta Research Laboratory, Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USALung and Placenta Research Laboratory, Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USALaboratory of Obesity and Metabolism, Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USALaboratory of Osteoarthritis and Inflammatory Diseases, Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USALung and Placenta Research Laboratory, Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USAApproximately 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.http://www.mdpi.com/1422-0067/18/3/652receptor for advanced glycation end-products (RAGE)secondhand smokediseaseexposure |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Joshua B. Lewis Kelsey M. Hirschi Juan A. Arroyo Benjamin T. Bikman David L. Kooyman Paul R. Reynolds |
spellingShingle |
Joshua B. Lewis Kelsey M. Hirschi Juan A. Arroyo Benjamin T. Bikman David L. Kooyman Paul R. Reynolds Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure International Journal of Molecular Sciences receptor for advanced glycation end-products (RAGE) secondhand smoke disease exposure |
author_facet |
Joshua B. Lewis Kelsey M. Hirschi Juan A. Arroyo Benjamin T. Bikman David L. Kooyman Paul R. Reynolds |
author_sort |
Joshua B. Lewis |
title |
Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure |
title_short |
Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure |
title_full |
Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure |
title_fullStr |
Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure |
title_full_unstemmed |
Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure |
title_sort |
plausible roles for rage in conditions exacerbated by direct and indirect (secondhand) smoke exposure |
publisher |
MDPI AG |
series |
International Journal of Molecular Sciences |
issn |
1422-0067 |
publishDate |
2017-03-01 |
description |
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. |
topic |
receptor for advanced glycation end-products (RAGE) secondhand smoke disease exposure |
url |
http://www.mdpi.com/1422-0067/18/3/652 |
work_keys_str_mv |
AT joshuablewis plausiblerolesforrageinconditionsexacerbatedbydirectandindirectsecondhandsmokeexposure AT kelseymhirschi plausiblerolesforrageinconditionsexacerbatedbydirectandindirectsecondhandsmokeexposure AT juanaarroyo plausiblerolesforrageinconditionsexacerbatedbydirectandindirectsecondhandsmokeexposure AT benjamintbikman plausiblerolesforrageinconditionsexacerbatedbydirectandindirectsecondhandsmokeexposure AT davidlkooyman plausiblerolesforrageinconditionsexacerbatedbydirectandindirectsecondhandsmokeexposure AT paulrreynolds plausiblerolesforrageinconditionsexacerbatedbydirectandindirectsecondhandsmokeexposure |
_version_ |
1725869372207005696 |