Hypothetical model of mitochondria–endoplasmic reticulum (ER) cross talk in asbestos-induced apoptosis. ER stress due to asbestos causes Ca2+ release and activation of an unfolded protein response (UPR), especially inositol-requiring kinase 1α (IRE-1α), which lead to activation of mitochondria-regulated apoptosis. Abbreviations: Akt, protein kinase B; ATF, activating transcription factor; BiP, binding immunoglobulin protein; CHOP, CCAAT/enhancer-binding protein homologous protein; eIF2α, eukaryotic initiation factor 2α; ERAD, endoplasmic reticulum–associated protein degradation; IP3R, inositol-1,4,5-triphosphate receptor; PERK, protein kinase RNA–like endoplasmic reticulum kinase; PML, promyocytic leukemia oncogenic protein; PTP, permeability transition pore; ROS, reactive oxygen species; XBP1, X box–binding protein 1. Modified from Reference 61.