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Updated: Sep 9, 2025

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Metabolismo lipídico anormal y aterosclerosis: una nueva perspectiva sobre la regulación de la función de los

Xize Wu1, Yuxi Huang1, Jiaqi Ren1

  • 1The First Clinical College, Liaoning University of Traditional Chinese Medicine, Shenyang, China.

Frontiers in immunology
|September 2, 2025
PubMed
Resumen

La progresión de la aterosclerosis implica ferroptosis impulsada por el metabolismo de los lípidos, que tiene un impacto en el microambiente inmune. Los genes clave como CYBB y HMOX1 regulan este proceso, ofreciendo objetivos terapéuticos potenciales.

Palabras clave:
la aterosclerosisLa bioinformáticaLa ferroposisLos lisosomasAprendizaje automáticoLas mitocondrias

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Área de la Ciencia:

  • Biología cardiovascular
  • Mecanismos de muerte celular
  • La medicina molecular

Sus antecedentes:

  • La aterosclerosis (AS) es una de las principales causas de enfermedades cardiovasculares, vinculada a la acumulación de lípidos.
  • La ferroptosis, una forma de muerte celular dependiente del hierro, es cada vez más reconocida como un factor clave en la patogénesis de la EA.
  • La comprensión de la ferroposis dentro del metabolismo lipídico es crucial para la investigación de la EA.

Objetivo del estudio:

  • Investigar los mecanismos de la ferroposis en el contexto del metabolismo de los lípidos en la aterosclerosis.
  • Identificar los genes clave que regulan la ferroposis y el metabolismo de los lípidos en la EA.
  • Explorar el impacto de estos genes en el microambiente inmune de la EA.

Principales métodos:

  • Análisis diferencial de la expresión génica y minería de conjuntos de datos (GSE100927).
  • Clustering, análisis de red de coexpresión de genes ponderados (WGCNA) y aprendizaje automático (LASSO, SVM-RFE, RF) para la identificación de genes Hub.
  • Validación in vitro utilizando modelos celulares inducidos por ox-LDL (HUVEC, RAW 264.7) y análisis de secuenciación de ARN de una sola célula.

Principales resultados:

  • Se identificaron seis genes de ferroptosis relacionados con el metabolismo de los lípidos de la aterosclerosis (ASLMRFeGs), que influyen en el microambiente inmune.
  • El aprendizaje automático identificó cuatro genes Hub candidatos (TYROBP, CSF1R, LCP2, C1QA).
  • Los estudios in vitro confirmaron que el metabolismo lipídico desregulado promueve la ferroptosis y su inhibición mejora la disfunción celular. Se identificaron cinco genes Hub validados (CYBB, HMOX1, IL1B, TYROBP, CSF1R), con una alta expresión en las células de espuma, los macrófagos, las células del músculo liso y las células T.

Conclusiones:

  • El metabolismo lipídico anormal en el SA impulsa la ferroposis a través de genes reguladores específicos (CYBB, HMOX1, IL1B, TYROBP, CSF1R).
  • Estos genes remodelan significativamente el microambiente inmune en la EA.
  • Los hallazgos ofrecen información sobre la patogénesis de la EA y las posibles estrategias terapéuticas dirigidas a la ferroptosis y el metabolismo lipídico.