Gestresste Mitochondrien: zwischen Zellschutz und Zelltod

Abstract Mitochondrial dysfunction is a hallmark of aging and important human diseases. Mitochondrial defects disturb protein import and lead to cytosolic accumulation of mitochondrial precursor proteins, disrupting cellular homeostasis. In human cells, this activates an integrated stress response to halt translation, and a heat shock response to counteract protein misfolding and aggregation. The interplay between these responses is critical for cellular fate in the face of mitochondrial perturbation.