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Acrolein Induces Inflammatory Response Underlying Endothelial Dysfunction
Author(s) -
Park Yong Seek,
Taniguchi Naoyuki
Publication year - 2008
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1433.034
Subject(s) - acrolein , p38 mitogen activated protein kinases , proinflammatory cytokine , protein kinase a , oxidative stress , endothelial dysfunction , inflammation , medicine , kinase , chemistry , cancer research , immunology , microbiology and biotechnology , biology , endocrinology , biochemistry , catalysis
Endothelial dysfunction by proinflammatory stimuli represents an important link between risk factors and the pathologic mechanisms underlying atherosclerosis. Thus, control of the inflammatory status of endothelial cells is crucial to limiting the disease. Tobacco smoking induces inflammatory reactions and promotes atherosclerosis; however, the mechanism that links cigarette smoking to an increased incidence of atherosclerosis is poorly understood. Our study demonstrates that acrolein, a known toxin in tobacco smoke, elevates oxidative stress via inactivation of thioredoxin reductase and stimulates expression of cyclooxygenase‐2 through activation of the protein kinase C, p38 mitogen‐activated protein kinase, and cAMP response element‐binding protein pathway in endothelial cells. Our finding suggests that acrolein may play a role in the progression of atherosclerosis.