Ronald Evans<\/a>;, Doctor en Medicina y Doctor en Filosof\u00eda. Los autores principales de los estudios fueron Peter Tontonoz, Doctor en Medicina y Doctor en Filosof\u00eda, y Laszlo Nagy, Doctor en Medicina y Doctor en Filosof\u00eda. <\/p>\nLos investigadores creen que la forma de colesterol responsable de promover la formaci\u00f3n de placas es la lipoprote\u00edna de baja densidad oxidada (oxLDL). Los estudios de Salk demuestran que la captaci\u00f3n de oxLDL por las c\u00e9lulas macrof\u00e1gicas activa un gen llamado PPARgamma (identificado previamente como un receptor involucrado en el desarrollo del tejido adiposo y el almacenamiento de grasa). Esta nueva comprensi\u00f3n sobre la funci\u00f3n de PPARgamma lo convierte en el segundo gen implicado en causar la aterosclerosis. <\/p>\n
Los estudios actuales demuestran que PPARgamma aumenta la producci\u00f3n de CD36, un receptor de superficie que importa oxLDL, estableciendo as\u00ed un ciclo de retroalimentaci\u00f3n positiva para el tr\u00e1fico de colesterol hacia la c\u00e9lula. Finalmente, el macr\u00f3fago se convierte en una \u201cc\u00e9lula espumosa\u201d, el primer tipo celular observado durante la formaci\u00f3n de placas ateroscler\u00f3ticas. <\/p>\n
El grupo Evans ha demostrado previamente que PPARgamma tambi\u00e9n es estimulado por las tiazolidinedionas, lo que plantea la pregunta de si los diab\u00e9ticos tipo II que toman estos medicamentos ampliamente recetados podr\u00edan tener un mayor riesgo de aterosclerosis. Esta es una pregunta importante, ya que muchos diab\u00e9ticos tienen sobrepeso y ya corren riesgo de enfermedades card\u00edacas. Seg\u00fan la American Diabetes Association, la diabetes tipo 2 afecta a aproximadamente 15 millones de estadounidenses, pero los investigadores instan a la cautela al interpretar los resultados anunciados hoy. <\/p>\n
\u201cLas c\u00e9lulas grasas y los macr\u00f3fagos en el h\u00edgado tambi\u00e9n producen CD36, lo cual es beneficioso para captar oxLDL y eliminarlo de la circulaci\u00f3n\u201d, dijo Nagy. \u201cPor lo tanto, un aumento en PPARgamma puede hacer m\u00e1s bien que mal. Lo que necesitamos hacer es averiguar c\u00f3mo modular el circuito de retroalimentaci\u00f3n PPARgamma\/CD36 localmente, espec\u00edficamente en las arterias\u201d.\u201d <\/p>\n
El art\u00edculo \u201cPPARgamma Promotes Monocyte\/Macrophage Differentiation and Uptake of Oxidized LDL\u201d es coescrito por Tontonoz, Nagy, Jacqueline G.A. Alvarez, Vilmos A. Thomazy, MD, PhD, y Evans. Nagy est\u00e1 en licencia de la Facultad de Medicina de la Universidad de Debrecen, Hungr\u00eda, y Thomazy trabaja en la Universidad de Texas en Houston. Tontonoz tiene una afiliaci\u00f3n conjunta con Salk y la Universidad de California, San Diego. El art\u00edculo \u201cOxidized LDL Regulates Macrophage Gene Expression through Ligand Activation of PPARgamma\u201d es coescrito por Nagy, Tontonoz, Alvarez, Hongwu Chen, PhD, y Evans. <\/p>\n
El Instituto Salk de Estudios Biol\u00f3gicos, ubicado en La Jolla, California, es una instituci\u00f3n independiente sin fines de lucro que realiza investigaci\u00f3n cient\u00edfica b\u00e1sica dedicada a la mejora de la salud humana y al aumento de la cantidad y calidad del suministro mundial de alimentos.<\/p>\n
Sus dos \u00e1reas principales de concentraci\u00f3n son neurociencia y biolog\u00eda molecular-celular y gen\u00e9tica; El Instituto Salk fue recientemente clasificado como la instituci\u00f3n de investigaci\u00f3n n\u00famero uno a nivel mundial en ambas \u00e1reas por el Instituto de Informaci\u00f3n Cient\u00edfica, con sede en Filadelfia.<\/p>\n
El Instituto Salk fue fundado en 1960 por Jonas Salk, MD, pionero de la vacuna contra la polio, con una donaci\u00f3n de terrenos por parte de la Ciudad de San Diego y el apoyo financiero de la March of Dimes Birth Defects Foundation. Thomas D. Pollard, MD, es el Presidente y Director Ejecutivo.<\/p>","protected":false},"featured_media":0,"template":"","faculty":[91],"disease-research":[],"class_list":["post-2212","disclosure","type-disclosure","status-publish","hentry","faculty-ronald-evans"],"acf":[],"yoast_head":"\n
Salk researchers find genetic feedback loop implicated in the early events of atherosclerotic plaque formation - Salk Institute for Biological Studies<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.salk.edu\/es\/news-release\/salk-researchers-find-genetic-feedback-loop-implicated-in-the-early-events-of-atherosclerotic-plaque-formation\/\" \/>\n<meta property=\"og:locale\" content=\"es_MX\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Salk researchers find genetic feedback loop implicated in the early events of atherosclerotic plaque formation - Salk Institute for Biological Studies\" \/>\n<meta property=\"og:description\" content=\"La Jolla, CA \u2013 Salk Institute scientists today announced two research findings related to the development of atherosclerosis. 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