PI3K as Mediator of Apoptosis and Contractile Dysfunction in TGFβ1-Stimulated Cardiomyocytes.

Paulin BrosinskyJulia BornbaumBjörn WargaLisa SchulzKlaus-Dieter Schlüter Alessandra Ghigo Emilio Hirsch Rainer Schulz Gerhild EulerJacqueline Heger

Published in: Biology (2021)

TGFβ1-induced SMAD activation, cardiomyocyte apoptosis, and impaired cell shortening are mediated via both, the ALK5 receptor and PI3K, in adult cardiomyocytes. PI3Kγ specifically contributes to apoptosis induction and impairment of contractile function independent of SMAD signaling.

Keyphrases

transforming growth factor
oxidative stress
endoplasmic reticulum stress
cell cycle arrest
high glucose
cell death
epithelial mesenchymal transition
diabetic rats
skeletal muscle
single cell
smooth muscle
stem cells
cell therapy
cell proliferation
mesenchymal stem cells
childhood cancer