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Video Experimental Relacionado

Updated: Jan 7, 2026

Two-photon Intravital Imaging of Leukocytes During the Immune Response in Lipopolysaccharide-treated Mouse Liver
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Sepsis e o fígado

Eleni V Geladari1, Anastasia-Amalia C Kalergi1, Apostolos A Evangelopoulos2

  • 13rd Department of Internal Medicine & Liver Unit, "Evangelismos" General Hospital, 45-47 Ipsilantou Str, 106 76 Athens, Greece.

Diseases (Basel, Switzerland)
|December 24, 2025
PubMed
Resumen

La lesión hepática asociada a sepsis (SALI) implica distintas fases inflamatorias e inmunosupresoras que afectan los resultados del paciente. La investigación tiene como objetivo desarrollar terapias personalizadas dirigidas a la inflamación, el metabolismo y el eje intestino-hígado para mejorar el manejo de SALI.

Palabras clave:
biomarcadoreseje intestino-hígadocascada inflamatoriadisfunción mitocondriallesión hepática asociada a sepsis (SALI)

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Área de la Ciencia:

  • Hepatología
  • Inmunología
  • Medicina de Cuidados Críticos

Sus antecedentes:

  • La lesión hepática asociada a sepsis (SALI) es una complicación crítica de la sepsis, caracterizada por distintas fases hiperinflamatoria e inmunosupresora.
  • Estas fases dictan los fenotipos de los pacientes e influyen en las estrategias terapéuticas.

Objetivo del estudio:

  • Caracterizar las distintas fases inflamatoria e inmunosupresora de SALI.
  • Establecer una base para el desarrollo de estrategias de inmunomodulación adaptadas a las respuestas inmunitarias individuales en la sepsis.

Principales métodos:

  • Revisión de la literatura existente sobre la patogénesis de SALI.
  • Análisis de vías celulares, alteraciones metabólicas y el eje intestino-hígado en la sepsis.
  • Evaluación de enfoques diagnósticos y terapéuticos actuales y en investigación.

Principales resultados:

  • La fase inflamatoria implica la activación de NF-κB y la inflamación NLRP3, lo que lleva a una tormenta de citoquinas, daño de hepatocitos y un mayor riesgo de mortalidad.
  • La fase inmunosupresora se caracteriza por un control deficiente de la infección, disfunción metabólica (por ejemplo, oxidación deficiente de ácidos grasos) y disfunción mitocondrial.
  • El eje intestino-hígado es central en la patogénesis de SALI, y la disbiosis y el aumento de la permeabilidad intestinal exacerban la lesión hepática; los biomarcadores novedosos muestran una promesa diagnóstica.

Conclusiones:

  • La investigación futura debe priorizar el desarrollo de modelos representativos y la validación de biomarcadores para SALI.
  • Se necesitan ensayos clínicos para permitir terapias personalizadas dirigidas a la inflamación, el metabolismo y el eje intestino-hígado.
  • Mejorar los resultados en SALI requiere un enfoque multifacético que aborde su compleja fisiopatología.