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El fibroblasto cardíaco glicogénico sintasa quinasa-3β regula la remodelación ventricular y la disfunción en el

Hind Lal¹, Firdos Ahmad¹, Jibin Zhou¹

¹From the Center for Translational Medicine (H.L., F.A., J.Z., J.E.U., R.J.V., Y.G., E.G., T.F.), Department of Clinical Sciences (D.Y.), and Section of Cardiology (E.J.T., T.F.), Temple University School of Medicine, Philadelphia, PA; Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada (J.W.); and Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, TN (H.L., F.A., Y.G., T.F.).

|June 6, 2014

Resumen

La inhibición de la glicógeno sintetasa quinasa-3β (GSK-3β) promueve la fibrosis cardíaca mediante la activación de los miofibroblastos y la señalización TGF-β1 / SMAD-3. La orientación GSK-3β puede tratar trastornos fibróticos del miocardio.

Área de la Ciencia:

Biología Cardiovascular Biología Cardiovascular
Investigación de la fibrosis en la investigación de la fibrosis.
Cardiología Molecular Cardiología Molecular

Sus antecedentes:

El infarto de miocardio (IM) causa remodelación cardíaca, incluida la fibrosis, que se entiende mal.
Las terapias actuales contra la fibrosis son insuficientes, lo que requiere nuevos objetivos moleculares.
Los fibroblastos cardíacos activados depositan la matriz extracelular después del infarto de miocardio, lo que contribuye a la fibrosis.

Objetivo del estudio:

Para investigar el papel de la glucógeno sintetasa quinasa-3β (GSK-3β) en la fibrosis miocárdica.
Identificar GSK-3β como un objetivo terapéutico potencial para la prevención de la fibrosis cardíaca.

Principales métodos:

Modelos de ratón de nocaut GSK-3β específicos para fibroblastos generados.
Se analizaron tejidos fibróticos de corazones de humanos y ratones después de un infarto de miocardio.
Investigó la interacción de GSK-3β con la señalización transformadora del factor de crecimiento-β1/SMAD-3.
Utilizó un inhibidor de molécula pequeña de SMAD-3.

Principales resultados:

Se encontró que la GSK-3β estaba fosforilada (inhibida) en los tejidos cardíacos fibróticos.
La eliminación de GSK-3β en los fibroblastos cardíacos indujo un fenotipo de miofibroblastos profibróticos.
GSK-3β inhibe directamente la actividad transcripcional SMAD-3, una vía profibrótica clave.
La inhibición de SMAD-3 evitó en gran medida la fibrosis y la remodelación ventricular izquierda limitada después del IM.

Conclusiones:

GSK-3β juega un papel inhibidor crítico en la activación de los fibroblastos cardíacos y la fibrosis.
Dirigirse a GSK-3β es una estrategia terapéutica prometedora para los trastornos fibróticos miocárdicos.
Los fibroblastos cardíacos son jugadores clave en la remodelación posterior al infarto de miocardio y la disfunción ventricular.

Palabras clave:

los fibroblastos en los que se encuentran.La fibrosis es una fibrosis.La glicogénica sintetasa quinasa 3 beta y la glicogénica sintetasa quinasa 3 beta también se encuentran presentes.La hipertrofia es una hipertrofia.Infarto de miocardio por infarto de miocardio

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