Biology · 2 authors, 1 centre
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This review summarizes the crosstalk between the integrated stress response (ISR), including stress granules, and regulated cell death pathways. The central result is that ISR and stress granules generally inhibit apoptosis, pyroptosis, and necroptosis to promote cell survival, but this mechanism can also be exploited by cancer cells and viruses.
This is a narrative review discussing molecular and cellular interactions between the integrated stress response (ISR), stress granules (SGs), and regulated cell death (RCD) pathways like apoptosis, pyroptosis, and necroptosis. The authors synthesize evidence from laboratory studies, including cell lines and animal models, showing that stress kinases (GCN2, PKR, PERK) phosphorylate eIF2α, leading to translational repression and SG assembly. SGs sequester pro-death components, inhibiting RCD and promoting survival. However, this pro-survival mechanism in stressed normal cells can be co-opted by cancer cells to withstand therapy or hypoxia, and by viruses to facilitate replication. The implications are that understanding these crosstalk mechanisms may reveal novel therapeutic targets for cancer and infectious diseases.
