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Use of non-invasive technology to evaluate active atheromatous lesions

AuthorsBoscá, Lisardo
Issue Date2013
CitationGEIRLI 2013
AbstractDuring development of atherosclerosis, ROS are key components in the outcome and nature of the constituents of the atheromatous lesion, defining a specific microenvironment (e.g. oxidized lipids, cytokines, hypoxia, et. ) that mediate monocyte/macrophage recruitment and a defined pro/anti-inflammatory phenotype. We have analyzed how macrophage proinflammatory activation and energetics are tightly linked under conditions relevant to atheroma, resulting in close titration of glycolysis relative to the degree of macrophage activation Multicomponent analysis including hypoxia and cytokine/chemokine determination define specific patterns of macrophage activation that are involved in the generation of the atheromatous lesion. In this way, we have analyzed the synergistic actions with oxidized lipids and cytokines, via a mechanism that depends on hypoxia inducible factor (HIF) and ubiquitous phosphofructokinase 2 (uPFK2). Further, we have demonstrated that selective impairment of uPFK2 or hypoxia sensing leads to decreased macrophage viability, and therefore an inappropriate resolution of the inflammatory response with cells filled with lipidic particles without an efficient export activity, typical of systems that avoid atheromatous development. These observations provide new fundamental mechanistic insights into the interrelationship between macrophage activation and energetics, and offer opportunities to develop novel therapeutic targets to alleviate atherosclerotic inflammation and its clinical complications.
DescriptionResumen del trabajo presentado a la VIII Reunión del Grupo Español de Investigación en Radicales Libres, celebrado en la Facultad de Medicina de la Universidad de Valencia del 3 al 5 de junio de 2013.
Appears in Collections:(IIBM) Comunicaciones congresos
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