Fig. 1
From: The different axes of the mammalian mitochondrial unfolded protein response
Folding stress responses. Protein misfolding activates transient, pro-survival stress responses that increase the folding capacity (i.e., modulation of chaperone and protease levels) and decrease the folding load (i.e., decrease in translation) to restore proteostasis. Responses typically last several hours. Prolonged stress activation that cannot alleviate the stress causes alternative outcomes, including cell death. Pharmacological induction of protein misfolding allows the study of the acute response to protein misfolding. Chronic activation of the stress, as observed upon genomic modulation or in disease, leads to the activation of alternative pathways and potentially cell death