Bounties attract serious brainpower to the challenge.
Mitochondrial dysregulation has always been considered as one of the many reasons for aging . But what if I tell you we can use it to prolong lifespan , just like Thanos said "I used the stones to destroy the stones", well it seems a distant reality but it has already been proved in mutants of C.elegans. The underlying hypothesis is that inhibiting cyc-2.1 (cytochrome)  in germline significantly extends lifespan by activating UPRmt and AMPK pathways.
Scientific analysis using translational profiling, scientists have identified that an RNA-binding protein GLD-1 acts as a key translational repressor of cyc-2.1 . Thus using RNA interference technique on C.elegans mutant daf-2 rsks-1 suppressed cyc-2.1 expression by inhibiting GLD-1 which is an critical transcriptional regulators of UPRmt . Thus, a cascade of signalling follows in which the insulin-like signaling and TOR pathway-mediates an tissue-specific translational repression of cytochrome c which induces the cell for an non-autonomous mitochondrial stress response that promotes longevity.
Imagine if we are able to reproduce the similar results in humans, as well!!!
Germline Signaling Mediates the Synergistically Prolonged Longevity Produced by Double Mutations in daf-2 and rsks-1 in C. elegans