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. Author manuscript; available in PMC: 2019 Jul 15.
Published in final edited form as: Mol Cell Endocrinol. 2017 Nov 7;470:240–250. doi: 10.1016/j.mce.2017.11.004

Fig 7-. Cartoon of regulation of KLF15 in cardiomyocytes to impact cardiac hypertrophy:

Fig 7-

AngII acting through TGFβ stimulates a TAK1-p38α kinase axis that inhibits KLF15 expression and nuclear localization of the protein. This contributes to increased gene expression and cardiomyocyte hypertrophy. ERβ acting through protein kinase A opposes TAK1-p38α activation. This restores KLF15 abundance and nuclear localization, contributing in part to inhibition of AngII-induced gene expression and cardiomyocyte hypertrophy.