ATF6 protects against protein misfolding during cardiac hypertrophy

Cardiomyocytes activate the unfolded protein response (UPR) transcription factor ATF6 during pressure overload-induced hypertrophic growth. The UPR is thought to increase ER protein folding capacity and maintain proteostasis. ATF6 deficiency during pressure overload leads to heart failure, suggesting that ATF6 protects against myocardial dysfunction by preventing protein misfolding. However, conclusive evidence that ATF6 prevents toxic protein misfolding during cardiac hypertrophy is still pending.

Source: Journal of Molecular and Cellular Cardiology - February 23, 2024 Category: Cytology Authors: Christoph Hofmann, Marjan Aghajani, Cecily D. Alcock, Erik A. Blackwood, Clara Sandmann, Nicole Herzog, Julia Gro ß, Lars Plate, R. Luke Wiseman, Randal J. Kaufman, Hugo A. Katus, Tobias Jakobi, Mirko Völkers, Christopher C. Glembotski, Shirin Doroudgar Source Type: research