Back

Intermittent hypoxia therapy engages multiple longevity pathways to double lifespan in C.elegans

Pitt, J. N.; Chavez, E.; Provencher, K. M.; Chen, M.; Tran, C.; Tran, J.; Huang, K.; Vaid, A.; Abadir, M. L.; Arang, N.; Leiser, S. F.; Roth, M. B.; Kaeberlein, M.

2022-10-17 physiology
10.1101/2022.10.13.512140 bioRxiv
Show abstract

Genetic activation of the hypoxia response robustly extends lifespan in C. elegans, while environmental hypoxia shows more limited benefit. Here we describe an intermittent hypoxia therapy (IHT) able to double the lifespan of wildtype worms. The lifespan extension observed in IHT does not require HIF-1 but is partially blocked by loss of DAF-16/FOXO. RNAseq analysis shows that IHT triggers a transcriptional state distinct from continuous hypoxia and affects down-stream genes of multiple longevity pathways. We performed a temperature sensitive forward genetic screen to isolate mutants with delayed nuclear localization of DAF-16 in response to IHT and suppression of IHT longevity. One of these mutations mapped to the enzyme Inositol Polyphosphate MultiKinase (IPMK-1). ipmk-1 mutants, like daf-16 mutants, partially suppress the benefits of IHT, while other effectors of phosphatidyl inositol signaling pathways (PLC{beta}4, IPPK, Go/i) more robustly suppress IHT longevity. One-Sentence SummaryIntermittent hypoxia therapy is frequency dependent, HIF independent, and requires FOXO, PLC{beta}, Go/i, IPMK, and IPPK.

Matching journals

The top 5 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.