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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Inflammation at the Molecular Interface of Atherogenesis </title><author><name sortKey="Lamon, Brian D" sort="Lamon, Brian D" uniqKey="Lamon B" first="Brian D." last="Lamon">Brian D. Lamon</name></author><author><name sortKey="Hajjar, David P" sort="Hajjar, David P" uniqKey="Hajjar D" first="David P." last="Hajjar">David P. Hajjar</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">18948435</idno><idno type="pmc">2570117</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570117</idno><idno type="RBID">PMC:2570117</idno><idno type="doi">10.2353/ajpath.2008.080442</idno><date when="2008">2008</date><idno type="wicri:Area/Pmc/Corpus">000073</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000073</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Inflammation at the Molecular Interface of Atherogenesis </title><author><name sortKey="Lamon, Brian D" sort="Lamon, Brian D" uniqKey="Lamon B" first="Brian D." last="Lamon">Brian D. Lamon</name></author><author><name sortKey="Hajjar, David P" sort="Hajjar, David P" uniqKey="Hajjar D" first="David P." last="Hajjar">David P. Hajjar</name></author></analytic><series><title level="j">The American Journal of Pathology</title><idno type="ISSN">0002-9440</idno><idno type="eISSN">1525-2191</idno><imprint><date when="2008">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Despite the multifactorial nature of atherosclerosis, substantial evidence has established inflammation as an often surreptitious, yet critical and unifying driving force which promotes disease progression. To this end, research has defined molecular networks initiated by cytokines, growth factors and other pro-inflammatory molecules which promote hallmarks of atherosclerosis such as endothelial dysfunction, macrophage infiltration, LDL oxidation, cell proliferation and thrombosis. Although commonly associated with risk factors such as dyslipidemia, diabetes and hypertension, the global etiology of atherosclerosis may be alternatively attributed to underlying anthropological pressures. The agricultural, industrial and technological revolutions produced alterations in dietary, social and economic factors which have collectively exaggerated the exposure of the human genome to environmental stimuli. Furthermore, advances in sanitation, nutrition, and medicine have increased the lifespan of humans, effectively prolonging blood vessel exposure to these factors. As a result, the vasculature has become conditioned to respond to injury with what is arguably an overzealous immunological response; thus setting the stage for the prevalence of cardiovascular disease, including atherosclerotic plaque development in Western populations. Evidence suggests that each of these alterations can be linked to specific mediators in the inflammatory process. Integration of these factors with an inflammation-based hypothesis of atherosclerosis has yet to be extrapolated to observations in the realms of basic and clinical sciences and is the focus of this review.</p></div></front></TEI><pmc article-type="review-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Am J Pathol</journal-id><journal-title>The American Journal of Pathology</journal-title><issn pub-type="ppub">0002-9440</issn><issn pub-type="epub">1525-2191</issn><publisher><publisher-name>American Society for Investigative Pathology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">18948435</article-id><article-id pub-id-type="pmc">2570117</article-id><article-id pub-id-type="doi">10.2353/ajpath.2008.080442</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Inflammation at the Molecular Interface of Atherogenesis </article-title><subtitle>An Anthropological Journey</subtitle></title-group><contrib-group><contrib contrib-type="author"><name><surname>Lamon</surname><given-names>Brian D.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Hajjar</surname><given-names>David P.</given-names></name></contrib><aff id="N0x1cdc680N0x38c63d0">From the Department of Pathology and Laboratory Medicine, Center of Vascular Biology, Weill Cornell Medical College of Cornell University, New York, New York</aff></contrib-group><pub-date pub-type="ppub"><month>11</month><year>2008</year></pub-date><volume>173</volume><issue>5</issue><fpage>1253</fpage><lpage>1264</lpage><history><date date-type="accepted"><day>5</day><month>8</month><year>2008</year></date></history><permissions><copyright-statement>Copyright © American Society for Investigative Pathology</copyright-statement><copyright-year>2008</copyright-year></permissions><self-uri xlink:title="pdf" xlink:href="zjh01108001253.pdf"></self-uri><abstract><p>Despite the multifactorial nature of atherosclerosis, substantial evidence has established inflammation as an often surreptitious, yet critical and unifying driving force which promotes disease progression. To this end, research has defined molecular networks initiated by cytokines, growth factors and other pro-inflammatory molecules which promote hallmarks of atherosclerosis such as endothelial dysfunction, macrophage infiltration, LDL oxidation, cell proliferation and thrombosis. Although commonly associated with risk factors such as dyslipidemia, diabetes and hypertension, the global etiology of atherosclerosis may be alternatively attributed to underlying anthropological pressures. The agricultural, industrial and technological revolutions produced alterations in dietary, social and economic factors which have collectively exaggerated the exposure of the human genome to environmental stimuli. Furthermore, advances in sanitation, nutrition, and medicine have increased the lifespan of humans, effectively prolonging blood vessel exposure to these factors. As a result, the vasculature has become conditioned to respond to injury with what is arguably an overzealous immunological response; thus setting the stage for the prevalence of cardiovascular disease, including atherosclerotic plaque development in Western populations. Evidence suggests that each of these alterations can be linked to specific mediators in the inflammatory process. Integration of these factors with an inflammation-based hypothesis of atherosclerosis has yet to be extrapolated to observations in the realms of basic and clinical sciences and is the focus of this review.</p></abstract></article-meta></front><floats-wrap><fig position="float" id="F1-7784"><label>Figure 1</label><caption><p>ECs, macrophages (Mϕ), SMCs, platelets, and B and T cells contribute to plaque development, potentially culminating in thrombosis. Vascular events depicted here are induced by inflammatory stimuli and occur in a cyclic manner to drive atherogenesis. Anthropological stimuli interject at multiple stages of lesion formation to enhance the inflammatory process during atherosclerosis. ECM, extracellular matrix.</p></caption><graphic xlink:href="zjh0110877840001"></graphic></fig><fig position="float" id="F2-7784"><label>Figure 2</label><caption><p>Hypothetical scheme of average life span at birth and fat intake (as percentage caloric intake) for select time periods. Data adapted from references.<xref rid="B1-7784" ref-type="bibr">1</xref>,<xref rid="B40-7784" ref-type="bibr">40</xref>,<xref rid="B46-7784" ref-type="bibr">46</xref></p></caption><graphic xlink:href="zjh0110877840002"></graphic></fig><fig position="float" id="F3-7784"><label>Figure 3</label><caption><p>Anthropological stimuli including nutritional characteristics, active versus sedentary lifestyles, socioeconomic class, and others dictate the expression profiles of our genome on two major levels. Chronically, these stimuli influence the widespread expression of genes, including the incorporation of beneficial mutations and the purging of undesirable genetic code. Acutely, these stimuli provoke a response that manifests as the genetic expression of an individual. Recent historical evidence demonstrates that changes in these stimuli have resulted in an amplified inflammatory response that collectively conditions and predisposes the vessel wall to plaque formation. Elucidation of these pathways at the genetic surface of populations, as well as individuals, will uncover multiple avenues of enhancing therapeutics, including risk stratification, lifestyle modifications, and personalized medicine, as well as the identification of inflammatory markers and molecular targets.</p></caption><graphic xlink:href="zjh0110877840003"></graphic></fig><table-wrap position="float" id="T1-7784"><label>Table 1</label><caption><p>Molecular Mediators of Inflammation Provoked by Anthropological Risk Factors as a Result of the Agricultural and Industrial Revolutions</p></caption><table frame="hsides" rules="groups"><thead><tr><th colspan="1" rowspan="1" align="center" valign="bottom">Anthropological risk factor</th><th colspan="1" rowspan="1" align="center" valign="bottom">Influence of agricultural and industrial revolutions</th><th colspan="1" rowspan="1" align="center" valign="bottom">Associated molecular mediators of inflammation (eg)</th></tr></thead><tbody><tr><td colspan="1" rowspan="1" align="left" valign="top">Energy intake</td><td colspan="1" rowspan="1" align="center" valign="top">↑</td><td colspan="1" rowspan="1" align="left" valign="top">TNF-α, CRP, ROS</td></tr><tr><td colspan="1" rowspan="1" align="left" valign="top">Total/saturated fat/trans fat</td><td colspan="1" rowspan="1" align="center" valign="top">↑</td><td colspan="1" rowspan="1" align="left" valign="top">TNF-α, COX-2, PGE<sub>2</sub>, MMP, ROS</td></tr><tr><td colspan="1" rowspan="1" align="left" valign="top">ω-6:ω-3 ratio</td><td colspan="1" rowspan="1" align="center" valign="top">↑</td><td colspan="1" rowspan="1" align="left" valign="top">ICAM, VCAM, selectins, PDGF, MMP, TXA<sub>2</sub>, ROS, ↓NO</td></tr><tr><td colspan="1" rowspan="1" align="left" valign="top">Salt</td><td colspan="1" rowspan="1" align="center" valign="top">↑</td><td colspan="1" rowspan="1" align="left" valign="top">MCP-1, PAI-1, COX-2, ROS</td></tr><tr><td colspan="1" rowspan="1" align="left" valign="top">Smoking</td><td colspan="1" rowspan="1" align="center" valign="top">↑</td><td colspan="1" rowspan="1" align="left" valign="top">ICAM, TNF-α, COX-2, PGE<sub>2</sub>, ROS</td></tr><tr><td colspan="1" rowspan="1" align="left" valign="top">Vitamins (A, E, C)</td><td colspan="1" rowspan="1" align="center" valign="top">↓</td><td colspan="1" rowspan="1" align="left" valign="top">ROS, IL-8, PAI-1</td></tr><tr><td colspan="1" rowspan="1" align="left" valign="top">Physical activity</td><td colspan="1" rowspan="1" align="center" valign="top">↓</td><td colspan="1" rowspan="1" align="left" valign="top">Cytokines, EPC, adiponectin</td></tr></tbody></table><table-wrap-foot><fn><p>TNF, tumor necrosis factor; CRP, C-reactive protein; ROS, reactive oxygen species; COX, cyclooxygenase; MMP, matrix metalloproteinase; MCP, monocyte chemoattractant protein; ICAM, intracellular adhesion molecule; VCAM, vascular cell adhesion molecule; PDGF, platelet-derived growth factor; NO, nitric oxide; PAI-1, plasminogen activator inhibitor; IL, interleukin; EPC, endothelial progenitor cell. </p></fn></table-wrap-foot></table-wrap></floats-wrap></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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