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La hiperlipidemia intermitente temprana altera los macrófagos del tejido para alimentar la aterosclerosis
Minoru Takaoka1, Xiaohui Zhao1, Hwee Ying Lim2,3
1Department of Medicine, Section of CardioRespiratory Medicine, University of Cambridge, Heart and Lung Research Institute, Cambridge, UK.
Nature
|September 4, 2024
Resumen
La exposición temprana al colesterol alto acelera la aterosclerosis al alterar los macrófagos arteriales, incluso con niveles acumulados similares de LDL-C. El control óptimo de la hiperlipidemia en la juventud es crucial para prevenir las enfermedades cardiovasculares.
Área de la Ciencia:
- Investigación cardiovascular
- Inmunología
- Enfermedad metabólica
Sus antecedentes:
- La hiperlipidemia es un factor de riesgo clave para la enfermedad cardiovascular aterosclerótica (ASCVD).
- La exposición temprana y fluctuante al colesterol de lipoproteína de baja densidad (LDL-C) aumenta de forma independiente el riesgo de ECPA.
- Los mecanismos que vinculan la hiperlipidemia precoz con el desarrollo acelerado de la EACV no se comprenden completamente.
Objetivo del estudio:
- Investigar el impacto de una dieta intermitente temprana con alto contenido de colesterol en el desarrollo de la aterosclerosis.
- Aclarar el papel de los macrófagos arteriales y las vías biológicas específicas en la EACV inducida por la dieta.
- Para correlacionar la exposición temprana al colesterol con la aterosclerosis a mediados de la edad adulta en humanos.
Principales métodos:
- Los ratones fueron alimentados con una dieta intermitente de alto colesterol de tipo occidental (WD) o con una dieta continua de WD.
- Análisis de las poblaciones de macrófagos arteriales, expresión génica y vías atheroprotectoras.
- Estudio longitudinal en humanos (Estudio de finlandeses jóvenes) para evaluar la exposición temprana al colesterol y el desarrollo de la placa carotídea.
Principales resultados:
- La alimentación temprana intermitente con WD aceleró la aterosclerosis en ratones a pesar de los niveles acumulados de LDL-C similares en comparación con la WD continua.
- Se observaron números y fenotipos alterados de macrófagos arteriales residentes en ratones expuestos temprano.
- Los macrófagos LYVE1+ fueron identificados como atheroprotectores, con vías de organización de actina implicadas en la aceleración de la aterosclerosis.
- La exposición temprana al colesterol en humanos se correlacionó significativamente con la incidencia y el tamaño de la placa carotídea a mediados de la edad adulta.
Conclusiones:
- La exposición intermitente temprana al colesterol es un determinante significativo de la aterosclerosis acelerada.
- Las alteraciones de los macrófagos arteriales y las vías celulares específicas son los mecanismos clave involucrados.
- El control de la hiperlipidemia temprano en la vida es crítico para la prevención de la EACV.
- Los hallazgos proporcionan información para el desarrollo de estrategias terapéuticas específicas contra la EACV.
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