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La fisión mitocondrial promueve la limpieza continua de las células apoptóticas por los macrófagos

Ying Wang1, Manikandan Subramanian2, Arif Yurdagul1

  • 1Department of Medicine, Columbia University, New York, NY 10032, USA.

Cell
|September 26, 2017
PubMed
Resumen

El aclaramiento eficiente de las células apoptóticas por los macrófagos requiere la fisión mitocondrial, un proceso crucial para prevenir la inflamación y enfermedades como la aterosclerosis. Este estudio revela cómo la proteína 1 relacionada con la dinamina (Drp1) impulsa la fisión mitocondrial para permitir la envoltura de múltiples células apoptóticas.

Palabras clave:
El DRP1Células apoptóticasla aterosclerosisseñalización del calcioEfeerocitosisLos macrófagosDinámica de las mitocondriasFisión de las mitocondriasLa fagocitosis

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Área de la Ciencia:

  • Biología celular
  • Inmunología
  • Dinámica de las mitocondrias

Sus antecedentes:

  • El aclaramiento celular apoptótico (eferocitosis) por los fagocitos es vital para prevenir la inflamación y el daño tisular.
  • La eferocitosis defectuosa está implicada en enfermedades como la aterosclerosis.
  • La eferocitosis eficiente requiere que los macrófagos internalicen múltiples células apoptóticas en secuencia.

Objetivo del estudio:

  • Investigar los mecanismos subyacentes a la capacidad de los macrófagos para la absorción de múltiples células apoptóticas.
  • Determinar el papel de la dinámica mitocondrial, específicamente la fisión, en la eferocitosis.

Principales métodos:

  • Investigó el papel de la proteína 1 relacionada con la dinamina (Drp1) en la mediación de la fisión mitocondrial durante la absorción celular apoptótica.
  • Se evaluó el impacto de la disfunción mitocondrial en los niveles de calcio citosólico y la formación de fagosomas.
  • Se utilizaron modelos de ratón (mieloide Drp1 knockout y Ldlr-/- ratones) para estudiar la eferocitosis in vivo.
  • Se examinaron los efectos de silenciar el uniporter de calcio mitocondrial (MCU).

Principales resultados:

  • La absorción celular apoptótica desencadena la fisión mitocondrial mediada por la proteína 1 relacionada con la dinamina (Drp1) en los macrófagos.
  • La inhibición de la fisión mitocondrial bloquea los aumentos de calcio y dificulta la formación de fagosomas para las células apoptóticas posteriores.
  • El silenciamiento del uniporter de calcio mitocondrial (MCU) rescata estos defectos de eferocitosis.
  • Los ratones que carecen de Drp1 mieloide presentan una eferocitosis deteriorada y fenotipos de enfermedad exacerbados en modelos de respuesta inmune y aterosclerosis.

Conclusiones:

  • La fisión mitocondrial, impulsada por Drp1, es esencial para permitir que los macrófagos engullan múltiples células apoptóticas.
  • Este proceso es crítico para mantener la homeostasis de los tejidos y prevenir las consecuencias patológicas de los defectos de eferocitosis.
  • Dirigirse a la fisión mitocondrial representa una estrategia terapéutica potencial para las enfermedades asociadas con la eferocitosis alterada.