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El 25-hidroxicolesterol derivado de los macrófagos promueve la inflamación vascular, la aterogénesis y la

Alberto Canfrán-Duque^1,2,3, Noemi Rotllan^1,2,3, Xinbo Zhang^1,2,3

¹Vascular Biology and Therapeutics Program (A.C.-D., N.R., X.Z., J.S., N.L.P., M.F.-F., J.W.F., W.C.S., G.T., C.F.-H., Y.S.).

|November 23, 2022

Resumen

El 25-hidroxicolesterol (25-HC), producido por los macrófagos, acelera la aterosclerosis al aumentar la inflamación y la inestabilidad de la placa. Este derivado del colesterol promueve la expresión de genes inflamatorios y la apoptosis, contribuyendo a la progresión de las enfermedades cardiovasculares.

Área de la Ciencia:

Biología cardiovascular
Metabolismo de los lípidos
Inmunología

Sus antecedentes:

El desarrollo de la aterosclerosis está influenciado por las interacciones entre el metabolismo de los esteroles y las vías inflamatorias.
Los derivados del colesterol, como el 25-hidroxicolesterol (25-HC), son reguladores clave de las respuestas inmunes de los macrófagos.
El papel preciso del 25-HC en la progresión de la aterosclerosis sigue siendo incompleto.

Objetivo del estudio:

Investigar la contribución del 25-hidroxicolesterol (25-HC) a la progresión de la aterosclerosis.
Aclarar los mecanismos por los que el 25-HC derivado de los macrófagos influye en el desarrollo y la estabilidad de la placa.

Principales métodos:

Niveles cuantificados de 25-HC y expresión de colesterol 25-hidroxilasa (CH25H) en placas ateroscleróticas.
Se utilizaron modelos quiméricos de médula ósea de ratón (tipo salvaje frente a knockout de Ch25h) trasplantados a ratones con deficiencia de Ldlr, seguidos de una alimentación con dieta occidental.
Se realizaron análisis lipidómicos y transcriptómicos in vitro de los macrófagos y se evaluó la migración de las células musculares lisas.

Principales resultados:

Se observaron niveles elevados de 25-HC en lesiones ateroscleróticas coronarias humanas.
El 25-HC derivado de los macrófagos aceleró la progresión de la aterosclerosis y promovió la inestabilidad de la placa.
El 25-HC amplificó las respuestas inflamatorias de los macrófagos, inhibió la migración de las células musculares lisas y alteró la señalización del receptor Toll-like 4.

Conclusiones:

El 25-HC derivado de los macrófagos promueve significativamente la aterogénesis amplificando los fenotipos inflamatorios.
El 25-HC contribuye a la inestabilidad de la placa a través de mecanismos autocrinos y paracrinos.
La producción o señalización de 25-HC puede ofrecer una estrategia terapéutica para la aterosclerosis.

Palabras clave:

la aterosclerosis inflamación Los macrófagos el oxicosterol

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