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Pkm2 Regula el ciclo celular de los cardiomiocitos y promueve la regeneración cardíaca

Ajit Magadum^1,2,3, Neha Singh^1,2,3, Ann Anu Kurian^1,2,3

¹Cardiovascular Research Center (A.M, N.S., A.A.K., I.M., T.M. K.B., M.T.K.S., E.C., Y.S., J.G.O., P.L, A.G.-S., C.K., M.M., L.Z.), Icahn School of Medicine at Mount Sinai, New York.

|February 21, 2020

Resumen

La isoenzima muscular piruvato quinasa 2 (Pkm2) promueve la actividad del ciclo celular de los cardiomiocitos y la regeneración cardíaca. La restauración de Pkm2 en el corazón adulto mejora la recuperación después del infarto de miocardio, ofreciendo un potencial terapéutico.

Área de la Ciencia:

Biología cardiovascular
Cardiología molecular
La Medicina Regenerativa

Sus antecedentes:

El corazón de los mamíferos adultos presenta una capacidad regenerativa limitada debido a la detención del ciclo celular de los cardiomiocitos.
La investigación está en curso para identificar los mecanismos que mejoran la regeneración miocárdica después del infarto de miocardio.
La función específica de la isoenzima 2 de la piruvato quinasa muscular (Pkm2) en la proliferación de los cardiomiocitos y la regeneración cardíaca sigue sin explorarse.

Objetivo del estudio:

Investigar la función de Pkm2 en la regulación del ciclo celular de los cardiomiocitos y la regeneración cardíaca.
Evaluar el impacto de la manipulación de Pkm2 en el desarrollo del corazón y la recuperación del infarto de miocardio.

Principales métodos:

Se utilizaron modelos de ratón con deleción de Pkm2 específica de los cardiomiocitos durante el desarrollo cardíaco (pérdida de función).
Se utilizó el ARNm modificado Pkm2 específico de los cardiomiocitos para estudios de ganancia de función.
Se evaluaron los efectos de Pkm2 en la proliferación de cardiomiocitos, la función cardíaca y la supervivencia después de un infarto de miocardio inducido.

Principales resultados:

Pkm2 se expresa en cardiomiocitos en desarrollo y neonatales, pero está regulado a la baja en adultos.
La deleción de Pkm2 alteró el ciclo celular de los cardiomiocitos, redujo el número de células y redujo el tamaño del miocardio.
La restauración de Pkm2 específica de los cardiomiocitos aumentó la división celular, mejoró la función cardíaca y aumentó la supervivencia después del infarto de miocardio.
Pkm2 regula el ciclo celular y mitiga el estrés oxidativo a través de las vías anabólicas y la β-catenina.

Conclusiones:

Pkm2 es un regulador intrínseco crítico del ciclo celular de los cardiomiocitos y el estrés oxidativo.
El ARN modificado Pkm2 específico de los cardiomiocitos representa una estrategia terapéutica prometedora para la regeneración cardíaca.

Palabras clave:

anabolismo Los cardiomiocitos Proliferación de las células regeneración

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