ArticleLife sciences2023
Canagliflozin shares common mTOR and MAPK signaling mechanisms with other lifespan extension treatments.
Article in Life sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- The tissue-specific effects of glucose-lowering drug targets on aging mediated through DNA methylation: a multi-omics genetic study.BMC medicine · 2026Article
- Sodium-glucose co-transporter 2 inhibition improves age-dependent kidney microvascular rarefaction.Kidney international · 2026Article
- An mTOR inhibitor discovery system using drug-sensitized yeast.GeroScience · 2025Article
- SGLT2 Inhibition Ameliorates Age-Dependent Renovascular Rarefaction.bioRxiv : the preprint server for biology · 2025Article
- Article
- Dapagliflozin ameliorates intestinal stem cell aging by regulating the MAPK signaling pathway inFrontiers in cell and developmental biology · 2025Article
- The lifespan-extending MEK1 inhibitor trametinib promotes regulation of de novo lipogenesis enzymes by chaperone-mediated autophagy.Frontiers in aging · 2025Article
- Late-life protein or isoleucine restriction impacts physiological and molecular signatures of aging.Nature aging · 2024Article
- Loss of 3-O-sulfotransferase enzymes, Hs3st3a1 and Hs3st3b1, reduces kidney and glomerular size and disrupts glomerular architecture.Matrix biology : journal of the International Society for Matrix Biology · 2024Article
- Lifespan effects in male UM-HET3 mice treated with sodium thiosulfate, 16-hydroxyestriol, and late-start canagliflozin.GeroScience · 2024Article
- Late-life isoleucine restriction promotes physiological and molecular signatures of healthy aging.bioRxiv : the preprint server for biology · 2024Article
- Chaperone-mediated autophagy as a modulator of aging and longevity.Frontiers in aging · 2024Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Long-lived mouse models and treatments that extend lifespan, such as Rapamycin, acarbose and 17α- -estradiol, lead to reduction in mTORC1 activity, declines in cap-dependent translation and increases in cap-independent translation. In addition, these treatments reduce the MEK-ERK-MNK (ERK1-2) signaling cascade, leading to reduction in eIF4E phosphorylation, which also regulates mRNA translation. Here, we report that Canagliflozin, a drug that extends lifespan only in male mice reduces mTORC1 and ERK1-2 signaling in male mice only. The data suggest reduction in mTORC1 and ERK pathways are common mechanisms shared by both genetic and pharmacological models of slowed aging in mice. Our data also reveal a significant sexual dimorphism in the ERK1-2 signaling pathway which might help to explain why some drugs can extend lifespan in males but have no effects in female mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.