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Investigación de la fibrosis renal inducida por TGF-β1 en un sistema paralelo computacional-experimental de

Kristin P Kim¹, Abigail Brooks¹, Christopher A Lemmon¹

¹Department of Biomedical Engineering, Virginia Commonwealth University, Richmond, VA, 23284, USA.

Biophysical journal

|February 1, 2026

Resumen

Este estudio utilizó modelos computacionales y cultivos celulares 3D para investigar la fibrosis renal. La inhibición del ensamblaje de fibronectina redujo eficazmente el daño tubular causado por el factor de crecimiento transformante beta 1.

Área de la Ciencia:

Nefrología
Biología Computacional
Biología Celular

Sus antecedentes:

La transición epitelio-mesénquima (EMT) y la remodelación de la matriz extracelular (MEC) impulsan la fibrosis renal.
La señalización del factor de crecimiento beta 1 (TGF-β1), regulada al alza por el ensamblaje de fibronectina (FN), promueve la EMT crónica y la fibrosis.
Los modelos tradicionales tienen dificultades para estudiar la interacción TGF-β1-FN y la organización de túbulos renales 3D en la fibrosis.

Objetivo del estudio:

Desarrollar y utilizar un enfoque computacional-in vitro combinado para investigar la interacción TGF-β1-FN en la fibrosis renal.
Modelar los efectos espaciales y temporales de las interacciones TGF-β1-FN en esferoides de células epiteliales tubulares 3D.
Evaluar el potencial terapéutico de la inhibición del ensamblaje de fibronectina en la fibrosis renal.

Principales métodos:

Desarrollo de un modelo computacional basado en agentes (ABM) que simula la fibrosis renal.
Empleo de esferoides de células epiteliales renales 3D para experimentos in vitro.
Investigación de los efectos de la estimulación con TGF-β1 y la inhibición del ensamblaje de fibronectina.

Principales resultados:

El ABM replicó con precisión la atrofia tubular y la remodelación de la matriz extracelular observadas en la fibrosis renal.
Las simulaciones del ABM predijeron que la inhibición del ensamblaje de la MEC prevendría la atrofia y la dilatación tubular.
Los experimentos in vitro con esferoides 3D confirmaron que la inhibición del ensamblaje de fibronectina mejoró la dilatación tubular inducida por TGF-β1.

Conclusiones:

Los modelos computacionales y los modelos in vitro 3D combinados ofrecen un enfoque potente para estudiar la fibrosis renal.
La inhibición del ensamblaje de fibronectina es una estrategia prometedora para contrarrestar el daño de los túbulos renales impulsado por TGF-β1.
La focalización del bucle de retroalimentación TGF-β1-FN puede ofrecer beneficios terapéuticos para la fibrosis renal.

Palabras clave:

fibrosis renal TGF-β1 fibronectina esferoides 3D modelado computacional terapia

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