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Fibrosis hepática y cáncer de hígado

Aina Anton¹, Scott Laurence Friedman², Bruno Cogliati^3,2

¹Institut d'Investigacions Biomèdiques August Pi i Sunyer, Centro de Investigación Biomédica en Red Enfermedades Hepáticas y Digestivas, Madrid, Spain.

Seminars in liver disease

|December 30, 2025

Resumen

La fibrosis hepática, no solo la cirrosis, puede iniciar el cáncer de hígado (carcinoma hepatocelular, VHC). La fibrosis remodela el microambiente hepático, promoviendo la inflamación y la inmunosupresión, impulsando el desarrollo del cáncer incluso antes de la cirrosis.

Área de la Ciencia:

Hepatología
Oncología
Inmunología
Gastroenterología

Sus antecedentes:

El carcinoma hepatocelular (VHC) a menudo surge en hígados fibróticos, siendo la cirrosis un factor de riesgo conocido.
La evidencia emergente indica que la fibrosis hepática, particularmente con la enfermedad del hígado graso asociada a disfunción metabólica (MASLD), puede impulsar la hepatocarcinogénesis independientemente de la cirrosis.
Las células estrelladas hepáticas (CEH) y el microambiente tumoral desempeñan papeles críticos en este proceso.

Objetivo del estudio:

Revisar las ideas mecanísticas que vinculan la fibrosis hepática con la iniciación del carcinoma hepatocelular (VHC).
Explorar los roles de la biología de las células estrelladas hepáticas (CEH) y la inmunología tumoral en la hepatocarcinogénesis impulsada por la fibrosis.
Destacar cómo la fibrosis crea un nicho premaligno que promueve el desarrollo del VHC.

Principales métodos:

Esta revisión sintetiza la literatura actual sobre la biología de las células estrelladas hepáticas (CEH) y la inmunología tumoral.
Se discuten los conocimientos mecanísticos sobre el remodelado de la matriz extracelular (MEC), la reprogramación de la vigilancia inmunitaria y la comunicación metabólica.
Se examina el papel del envejecimiento y la senescencia celular en la amplificación de las señales protumorales.

Principales resultados:

El remodelado del hígado fibrótico aumenta la rigidez de la matriz extracelular (MEC), altera la arquitectura hepática y promueve la angiogénesis anormal.
Las células estrelladas hepáticas (CEH) reprograman el microambiente inmunitario, lo que conduce a la exclusión de células inmunitarias y la inmunosupresión.
El envejecimiento y la senescencia exacerban la inflamación asociada a la fibrosis y la disfunción inmunitaria, reforzando la stemness y la resistencia a la terapia.

Conclusiones:

La fibrosis actúa como un instigador crítico del VHC al crear un microambiente permisivo para la transformación maligna.
La interacción entre la señalización fibrogénica, la desregulación inmunitaria y los factores metabólicos impulsa el desarrollo del VHC.
La comprensión de estos mecanismos revela posibles dianas terapéuticas para la prevención y el tratamiento del VHC.

Palabras clave:

fibrosis hepática cáncer de hígado carcinoma hepatocelular microambiente tumoral inmunosupresión células estrelladas hepáticas senescencia celular terapias dirigidas

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