The mitochondrial permeability transition pore activates the mitochondrial unfolded protein response and promotes aging

Mitochondrial activity determines aging rate and the onset of chronic diseases. The mitochondrial permeability transition pore (mPTP) is a pathological in inner membrane thought to be composed F-ATP synthase (complex V). OSCP, subunit synthase, helps protect against mPTP formation. How destabilization OSCP may contribute aging, however, unclear. We have found that loss nematode Caenorhabditis elegans initiates shortens lifespan specifically during adulthood, part via initiation unfolded protein response (UPR mt ). Pharmacological or genetic inhibition inhibits UPR restores normal lifespan. Loss putative pore-forming component extends adult lifespan, suggesting normally promotes aging. Our findings reveal how an mPTP/UPR nexus age-related diseases protective under certain conditions.