Christoph Hofmann, Marjan Aghajani, Cecily D Alcock, Erik A Blackwood, Clara Sandmann, Nicole Herzog, Julia Groß, Lars Plate, R Luke Wiseman, Randal J Kaufman, Hugo A Katus, Tobias Jakobi, Mirko Völkers, Christopher C Glembotski, Shirin Doroudgar
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. Here, we found that activation of the UPR, including ATF6, is a common response to pathological cardiac hypertrophy in mice...
February 23, 2024: Journal of Molecular and Cellular Cardiology