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La deficiencia de proteína quinasa dependiente de ARN de doble cadena protege el corazón de la insuficiencia cardíaca

Huan Wang¹, Xin Xu, John Fassett

¹Cardiovascular Division and Lillehei Heart Institute (H.W., X.X., J.F., D.K., X.L., X.H., R.J.B., Y.C.) and Pulmonary Division (P.B.), University of Minnesota Medical School, Minneapolis; Shanghai Tenth People's Hospital of Tongji University, Shanghai, China (X.L.); Institute of Molecular Medicine, Peking University, Beijing, China (X.H.); Ottawa Hospital Research Institute, Ottawa, ON, Canada (T.J.F., J.C.B.); and Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China (H.L.).

|January 28, 2014

Resumen

La proteína quinasa dependiente de ARN de doble cadena (PKR) promueve la insuficiencia cardíaca. La inhibición de la PKR en ratones con sobrecarga de presión redujo la inflamación, la apoptosis y la fibrosis, protegiendo contra el desarrollo de insuficiencia cardíaca congestiva.

Área de la Ciencia:

Biología Cardiovascular Biología Cardiovascular
La medicina molecular es una medicina molecular.
La señalización celular.

Sus antecedentes:

La proteína quinasa dependiente de ARN de doble cadena (PKR) regula la traducción del ARNm y la señalización inflamatoria.
La insuficiencia cardíaca congestiva (ICF) incluye hipertrofia de cardiomiocitos, inflamación y apoptosis.
El papel de la PKR en la patogénesis de la CHF no se había examinado previamente.

Objetivo del estudio:

Investigar el papel de la PKR en el desarrollo de la hipertrofia ventricular izquierda y CHF.
Para determinar si la inhibición de la PKR confiere protección contra la insuficiencia cardíaca inducida por sobrecarga de presión.

Principales métodos:

La expresión y localización de PKR se evaluaron en corazones humanos y ratones con insuficiencia cardíaca congestiva.
El knockout de PKR y los ratones de tipo salvaje se sometieron a una constricción aórtica transversal (TAC) para inducir una sobrecarga de presión.
La función cardíaca, la fibrosis, la inflamación y los marcadores de la apoptosis se evaluaron después del CTA.

Principales resultados:

La expresión de PKR miocárdico aumentó en CHF. Los ratones knockout de PKR mostraron una función cardíaca preservada y una fibrosis reducida después del TAC en comparación con el tipo salvaje.
El knockout de PKR atenuó la inflamación y la expresión del factor proapoptótico, lo que confiere resistencia a la apoptosis de los cardiomiocitos.
Agotamiento de la PKR en cardiomiocitos aislados protegidos contra la apoptosis inducida por TNF-α o LPS.

Conclusiones:

La PKR se regula al alza durante la sobrecarga hemodinámica y contribuye a la remodelación cardíaca desadaptativa.
La PKR promueve la inflamación del miocardio, la apoptosis de los cardiomiocitos y la progresión de la insuficiencia cardíaca congestiva.
La orientación de la PKR puede representar una estrategia terapéutica para prevenir o tratar la insuficiencia cardíaca.

Palabras clave:

La apoptosis es la apoptosis.La insuficiencia cardíaca es insuficiencia cardíaca.La inflamación es la inflamación de la inflamación.La inmunidad innata es la inmunidad.Las kinasas proteicas R y R.Iniciación de la traducción iniciación de la traducción.Reglamento de traducción Reglamento de traducción.

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