Fig. 4: ER stress induced by MFN2 depletion

Mfn2 ablation induces the activation of UPR proteins located in ER membranes. In particular, MFN2 has been proposed as an upstream modulator of PERK that under basal conditions maintains the kinase inactive. Once activated, UPR works by expanding the ER, upregulating chaperones and inhibiting protein translation. Mitochondria display higher Ca²⁺ uptake and ATP production to support the higher energy demand. It is still unclear whether Mfn2 ablation induces an increase or decrease of ER stress-induced apoptosis