ALTERACIONES EN LA HOMEOSTASIS DEL COLESTEROL HEPÁTICO Y SUS IMPLICACIONES EN LA ESTEATOHEPATITIS NO ALCOHÓLICA © 2017 Universidad Nacional Autónoma de México, Facultad de Estudios Superiores Zaragoza[.]
Trang 1Este es un artículo Open Access bajo la licencia CC BY-NC-ND (http://creativecommons.org/licenses/by-nc-nd/4.0/).
TIP Revista Especializada en Ciencias Químico-Biológicas, 20(1): 50-65, 2017.
DOI: 10.1016/j.recqb.2016.11.005
1 Programa de Doctorado en Ciencias Bioquímicas, Facultad de Química, Universidad Nacional Autónoma de México (UNAM), Ciudad Universitaria, Deleg Coyoacán, C.P
04510, Ciudad de México, México 2 Unidad de Genómica de Poblaciones Aplicada
a la Salud, Facultad de Química, UNAM/Instituto Nacional de Medicina Genómica (INMEGEN), Periférico Sur No 4809, Colonia Arenal Tepepan, Deleg Tlalpan, C.P
14610, Ciudad de México, México E-mail: badillo160682@hotmail.com
Nota: Artículo recibido el 18 de mayo de 2016 y aceptado
el 28 de septiembre de 2016
RESUMEN
Diversos estudios han demostrado que el colesterol libre (CL) hepático tiene una participación importante
en la patogénesis de la esteatohepatitis no alcohólica (EHNA) Estos estudios han proporcionado evidencias
de que la acumulación en el hígado de CL es tóxico a distintos niveles incluyendo: daño oxidativo a la mitocondria, estrés del retículo endoplasmático (RE) y activación de células de Kupffer (CKs) y células estelares hepáticas (CEH) En conjunto, estas evidencias sugieren que el contenido de CL hepático es importante en HOLQLFLRPDQWHQLPLHQWR\PRGXODFLyQGHODUHVSXHVWDLQÁDPDWRULDDVRFLDGDDOD(+1$(QHVWDUHYLVLyQVH discuten los distintos mecanismos participantes en la regulación de la homeostasis del colesterol y sus posibles implicaciones en el desarrollo y progresión del hígado graso no alcohólico (HGNA).
Palabras Clave: FROHVWHUROOLEUH(+1$¿EURVLV+*1$KRPHRVWDVLV.
Dysregulation in hepatic cholesterol homeostasis and its implications in nonalcoholic steatohepatitis
ABSTRACT
Several studies have shown that hepatic free cholesterol (FC) has an important role in the pathogenesis of nonalcoholic steatohepatitis (NASH) These studies have provided evidence that hepatic FC accumulation
is toxic at different levels including: mitochondrial oxidative injury, endoplasmic reticulum (ER) stress, and activation of Kupffer cells (KCs) and hepatic stellate cell (HSCs) Altogether, this suggests that hepatic FC FRQWHQWLVLPSRUWDQWIRUWKHLQLWLDWLRQPDLQWHQDQFHDQGPRGXODWLRQRIWKHLQÁDPPDWRU\UHVSRQVHDVVRFLDWHG with NASH In this review several mechanisms that participate in the regulation of cholesterol homeostasis and their possible implications in the development and progression of nonalcoholic fatty liver disease (NAFLD) are discussed.
Key Words: IUHHFKROHVWHURO1$6+¿EURVLV1$)/'KRPHRVWDVLV.
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